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    Blocking Interleukin-15 May Treat Celiac Disease Symptoms


    Jefferson Adams
    Image Caption: New study on blocking Interleukin-15 to treat celiac disease symptoms

    Celiac.com 03/18/2011 - By blocking an inflammatory protein called interleukin-15 (IL-15), doctors may be able to treat and prevent symptoms of celiac disease in some people, according to a new study in the journal Nature.


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    The data suggest that the inflammatory response to gluten in people with celiac disease may be triggered by interleukin-15 and retinoic acid, which is a derivative of vitamin A.

    The team notes that researchers previously thought that retinoic acid would lessen the inflammation in the intestine. Instead their study showed that it might actually worsen inflammation.

    According to Bana Jabri, MD, PhD, a member of the Celiac Disease Center and Comprehensive cancer Center at the University of Chicago, the team results showed that "elevated levels of IL-15 in the gut could initiate all the early stages of celiac disease in those who were genetically susceptible, and that blocking IL-15 could prevent the disease in our mouse model. It also demonstrated that in the treatment of inflammatory intestinal diseases, vitamin A and its retinoic acid metabolites are likely to do more harm than good.”

    The researchers found that by blocking IL-15 in mice that were genetically engineered to have celiac disease, they were able to reverse the symptoms, and the mice were able to eat gluten without suffering the symptoms of celiac disease.

    One reason this is good news, is that a number of medicines designed to block IL-15 are already being developed for other inflammation related diseases, such as rheumatoid arthritis.

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    Guest jim bindon

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    Excellent information. keep it coming. Thank you

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    Guest darlene

    Posted

    By blocking the symptoms are we getting rid of the disease or just masking what the disease does to the body..that frightens me...most medicines today for anything in regular medical world will mask the symptoms..not get rid of..or prevent disease...

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    Guest Linda

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    Any and all research is welcome and needed.

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    Guest Kristy Seifert

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    Great to hear such encouraging news. Thanks for passing it along.

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    Guest Helen Haas

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    Anything that can help the situation is a plus, hope to hear more good news on celiac.

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    Guest Patty Cook

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    I am excited to hear more about this......keep the news coming.

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    I appreciate this article. No more cod liver oil for me? How do we test levels?

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    Guest Beth Crow

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    Hi, good article, so we should stay away from vitamin A?

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    Guest Michael

    Posted

    Immune responses induced by Pelargonium sidoides extract in serum and nasal mucosa of athletes after exhaustive exercise: modulation of secretory IgA, IL-6 and IL-15.

     

    Phytomedicine. 2011 Feb 15;18(4):303-8

     

    Authors: Luna LA, Bachi AL, Novaes e Brito RR, Eid RG, Suguri VM, Oliveira PW, Gregorio LC, Vaisberg M

     

    Abstract

    The evidence that exhaustive exercise may compromise the immune response is mainly confirmed by upper respiratory tract infections which are probably related to the decrease in secretory immunoglobulin A in the upper airway mucosa and/or profile changes of systemic cytokines as well as local cytokines of the upper respiratory tract. An extract from Pelargonium sidoides roots is currently used to treat infections in the upper airways. The aim of the present study was to evaluate the action of this herbal medicine on the immune response of athletes submitted to an intense running session by analyzing the production of immunoglobulin A in their saliva and of cytokines both locally and systemically, using a placebo as control. The results show that Pelargonium sidoides extract modulates the production of secretory immunoglobulin A in saliva, both interleukin-15 and interleukin-6 in serum, and interleukin-15 in the nasal mucosa. Secretory immunoglobulin A levels were increased, while levels of IL-15 and IL-6 were decreased. Based on this evidence, we suggest that this herbal medicine can exert a strong modulating influence on the immune response associated with the upper airway mucosa in athletes submitted to intense physical activity.

    PMID: 20850953 [PubMed - indexed for MEDLINE]

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  • About Me

    Jefferson Adams is a freelance writer living in San Francisco. He has covered Health News for Examiner.com, and provided health and medical content for Sharecare.com. His work has appeared in Antioch Review, Blue Mesa Review, CALIBAN, Hayden's Ferry Review, Huffington Post, the Mississippi Review, and Slate, among others.

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  • Related Articles

    Roy Jamron
    This article originally appeared in the Spring 2004 edition of Celiac.com's Scott-Free Newsletter.
    Celiac.com 05/10/2004 - Identical twins enter life from the same womb sharing the same genetic code, the same family, the same home, largely experiencing the same environment as they develop from infancy through childhood and mature into adults. When celiac disease strikes one identical twin, the odds are the other twin also has celiac disease. Twin studies lead to the conclusion that celiac disease is strongly linked to genetic factors. Yet one identical twin may develop celiac disease while the other twin may remain completely free of celiac disease for decades if not for a lifetime.
    One study looked at 20 pairs of identical twins and 27 pairs of fraternal twins where at least one twin of the pair was known to have celiac disease. In 75% of the pairs of identical twins, both twins had celiac disease. In contrast, in only 11% of the pairs of fraternal twins did both twins have celiac disease. However, in 25% of the 20 identical twin pairs studied, one twin of the pair did not have celiac disease1. In another study which followed 5 pairs of female identical twins for 11-23 years (at least one twin of the pair having celiac disease or dermatitis herpetiformis), it was found that two of the twins who began the study with neither celiac disease or dermatitis herpetiformis remained free of the disease throughout the study2. In other words, something beyond genetics, some environmental factor, seems to be responsible for the onset of celiac disease. Exactly what is it that makes one twin intolerant to gluten and not the other?
    Looking for Answers
    To find an answer, one might start by asking when do signs of an intolerance to gluten first begin to emerge? A recent study in the UK looked at a screened sample of 5,470 children aged 7 years old and found 54 who tested positive for both tTG antibodies and IgA-EMA (tissue transglutaminase and antiendomysial antibodies) indicating celiac disease is likely present. This 1% prevalence in children is comparable to the 1% prevalence of celiac disease in adults in the UK. Since the prevalence of celiac disease is not greater in adults, this suggests that the onset of celiac disease begins in early childhood, even in cases where celiac disease is not diagnosed until later in adulthood. The authors of this study concluded, “The search for the trigger resulting in the breakdown of immune tolerance to gluten therefore needs to focus on infancy and intrauterine life3.”
    Breast-Feeding
    Breast-feeding has long been thought to delay or reduce the risk of developing celiac disease in children. This effect has been attributed to a number of potentially protective milk components and antibodies passed from the mother. Studies relying on questionnaires have found that the onset of celiac disease in children is significantly delayed if gluten is introduced into the diet while the child is still being breast-fed4-7. The effect of epidermal growth factor (EGF), a component of breast milk, was studied in newborn rats. Interferon-gamma and gliadin, a gluten protein, were administered to rat pups to induce gluten enteropathy. Celiac disease-like villus atrophy was found in rat pups fed an artificial milk diet without EGF but not in breast-fed pups or pups supplemented with EGF8. Recent research shows that breast milk also passes bacterial flora from mother to newborn9. Growth factors found in human milk have been shown to aid in establishing predominant species of commensal bacteria in the gut of breast-fed infants10. The makeup of microflora which colonize the gut in early infancy is dependant on many factors, including whether babies are bottle-fed or exclusively breast-fed, whether or not delivered by caesarean section, on treatment in neonatal intensive care units, hygienic conditions, and antimicrobial procedures. Initially, it is the maternal microflora that is the source of bacteria for the newborn gut. A diet of breast milk induces the development of a flora rich in Bifidobacterium in full-term infants11. The possibility that these microflora play critical symbiotic roles in the development of the intestine and its immunological functions has not yet been considered as a factor in the onset of celiac disease.
    The Beneficial Roles of Gut Bacteria
    Over 500 species of bacteria may be present in the human gut in concentrations of between 100 billion to 1 trillion microbes per gram adding up to about 95% of the total number of cells in the human body12,13. For many years it has been known that gut bacteria play an important and beneficial role in one’s health. Extraordinary new findings on how commensal microflora participate in early gut development and in the development of the immune system have been uncovered by recent research. Here is sampling of some of these discoveries:
    A study of 64 healthy formula and breast-fed infants, aged 0-6 months, examined fecal samples for intestinal colonization of Bacteriodes fragilis, Bifidobacterium-like, and Lactobacillus-like bacteria, and compared these results with counts of IgA, IgM, and IgG antibody-secreting cells in blood fluids drawn from the infants. The result was that infants colonized with B. fragilis at one month of age had significantly higher counts of IgA- and IgM-secreting cells at the age of two months than infants not colonized with B. fragilis. It was concluded that colonization timing and the type of bacteria colonizing the gut of newborns may influence the maturation of the naive immune system14.
    Bacteriodes thetaiotaomicron, a species abundant in the guts of humans and mice, has been the focus of much research, chosen because of its predominance in the microflora and ability to be genetically manipulated. Studies of this microbe introduced into the developing guts of gnotobiotic (germ-free) laboratory mice have found B. thetaiotaomicron seems to communicate with host cells in the intestine, altering and influencing gut development and function.
    One study has shown gene activity in the host is affected by B. thetaiotaomicron colonization. Using sophisticated DNA microarray devices, a comparison of gene expression of some 25,000 mouse genes was made between germ-free and B. thetaiotaomicron colonized mice. The activity of 118 genes was found to be increased or reduced by colonization. These genes are involved in several important intestinal functions, including nutrient absorption, intestinal permeability, toxin neutralization, intestinal blood vessel development, and postnatal gut maturation suggesting that these functions should be examined further in future studies15.
    An influence on fructose production in the gut by B. thetaiotaomicron was the first finding uncovered by researchers. Pre-weaned mice produce fructose sugar on the surface of cells lining the intestine providing a food source helping to establish commensal bacteria. B. thetaiotaomicron colonizing the gut of germ-free mice causes intestinal cells to continue fructose production after weaning. If B. thetaiotaomicron is not present after weaning, fructose synthesis stops. B. thetaiotaomicron actually senses when its supply of fructose is low and instructs the host to produce more fructose in response16.
    Gene activity findings led researchers to look at the development of the intricate network of intestinal blood vessels in mice raised germ-free and in mice raised colonized with B. thetaiotaomicron or normal gut flora. When the mice reached adulthood, capillary development in the intestines was examined. Capillary development in mice colonized with B. thetaiotaomicron or normal flora was normal and complex, but capillary development in the germ-free mice was immature and arrested. Further, it was, found for blood vessel development to occur, these microbes must interact with Paneth cells (epithelial cells located at the base of the “crypts” in the small intestine)17.
    The relationship of B. thetaiotaomicron with Paneth cells was further studied. It was discovered that Paneth cells produce a protein called angiogenin 4 or Ang4 and that Paneth cells are induced to express Ang4 by B. thetaiotaomicron. Ang4 and other angiogenins were found to exhibit bactericidal and fungicidal activities against certain known pathogens. It appears that B. thetaiotaomicron and other commensal microbes, which are themselves resistant to Ang4, take part in shaping the microbial ecology of the gut and innate immunity18.
    Another study found a relationship between commensal bacteria and the development of gut-associated lymphoid tissue (GALT) in rabbits. GALT consists of lymphocytes and organized tissues called Peyer’s patches and mesenteric lymph nodes (MLNs) located within the intestinal mucosa, which are involved in the induction of immunity and tolerance. During the first few months after birth, newborn animals and humans rely on antibodies passed maternally to fend off infections until the immune system can mature. After those first few months, a diversification of antibody repertoire normally takes place within the GALT. When, shortly after birth, the appendices of rabbits are tied-off and isolated to prevent colonization by microflora, GALT development within the appendices is arrested. Rabbit pups delivered sterilely, isolated and hand-reared on a sterile diet exhibited underdeveloped GALT and antibody repertoires. In further experimentation, a number of different bacteria species were introduced into surgically-rendered, germ-free appendices of rabbits. No bacteria species alone promoted GALT development. However, the combination of Bacteroides fragilis and Bacillus subtilis consistently resulted in the development of GALT and antibody repertoire. The conclusion is that specific combinations of microflora are required for GALT development19,20.
    In other research, the composition of commensal flora in rats was shown to alter intestinal permeability. Colonization with Escherichia coli, Klebsiella pneumoniae, and Streptococcus viridans significantly increased colonic wall permeability while colonization with the common probiotic strain, Lactobacillus brevis, significantly reduced permeability of the colon wall. Bacteroides fragilis induced only a slight permeability reduction21.
    Gut pathogens in combination with stimulation by cytokines such as TNF-alpha (tumor necrosis factor) can cause cells of the intestinal epithelium to respond by releasing proinflammatory cytokines like interleukin-8 (IL-8). A study found that probiotic strains, Bifidobacterium longum and Lactobacillus bulgaricus, can suppress IL-8 secretion in intestinal epithelia when stimulated by proinflammatory cytokines. Hence, some probiotic strains of bacteria may be able to down-regulate inflammation in the gut22.
    Other beneficial functions of microflora include the fermentation and removal of non-digestible dietary residue and the mucus residue produced by the epithelia; the derivation of energy as short-chain fatty acids by fermentation of carbohydrates in the colon; the production of vitamins, particularly those of the B group and vitamin K; the absorption of minerals and ions including calcium, magnesium and iron; and the formation of a protective functional barrier against pathogens23,24.
    A Role for Bacteria in Celiac Disease?
    As can been seen, commensal microflora play a myriad of complex, diverse and important roles in normal health and development. Much remains to be investigated, and new roles and functions microflora play are waiting to be discovered. The possibility that commensal bacteria are involved in the pathogenesis of celiac disease cannot be overlooked. Certainly, differences in the mix of microflora could account for why one identical twin may develop celiac disease while the other does not. Could the mix of commensal bacteria in newborn infants set the stage for the development of celiac disease? Could the onset of celiac disease be triggered by an event such as illness, use of antibiotics, stress, or pregnancy which alters the mix of microflora opening the door to a pathogenic interaction with gluten? One recent study has already found an association between antibiotic use and the development of Crohn’s disease25.
    Over the course of the last few years, much new understanding of the pathogenesis of celiac disease has come to light, but a fundamental question remains unanswered: Why does the immune system fail to tolerate gluten in some people? A possible mechanism involving one or more unidentified species of commensal bacteria possibly explaining why tolerance to gluten fails will be proposed and discussed here.
    Tolerance and Immunity
    The subject of tolerance and immunity is involved and complex, and science remains far from fully comprehending its workings. At heart, is how the immune system decides to react when an antigen is first presented to a naive T cell. The response of the immune system to an antigen is mediated and regulated by cell secretions of numerous proteins called “cytokines” sensed by a multitude of receptors on the various specialized cells of the immune system. Structural components of pathogens are also sensed by immune cell receptors called “Toll-like receptors”. Antigens may be any substance foreign to the body and may or may not actually be harmful. They could be components of food, or could be components of either friendly or pathogenic organisms.
    In celiac disease, the antigens are those gluten peptides which survive the process of digestion. In the current understanding of celiac disease, these peptides are transported across the mucosal epithelium as polypeptides. In mainly the subepithelial region, gluten peptides undergo a process called deamidation by an enzyme called tissue transglutaminase (tTG). A peptide is a chain of amino acids. Deamidation is a process that converts glutamine amino acid components of a gluten peptide into glutamic acid components. In the lamina propria region of the intestines, deamidated gluten peptides are taken up by antigen presenting cells called dendritic cells and presented by HLA-DQ2 or -DQ8 molecules on the surface of dendritic cells to receptors of gluten-sensitive naive CD4+ T cells (Note celiac disease here refers to a “cluster of differentiation” number, a numbering system for the cell-surface molecules which identify T cell type). Activated CD4+ T cells then differentiate and proliferate. Some T cells interact with B cells which, in turn, then differentiate into plasma cells producing antigliadin, antiendomysial and anti-tTG antibodies. Other T cells become natural killer or cytotoxic T cells, secreting cytokines which cause inflammation and damage to the enterocytes in the epithelium. Connective tissue cells called “fibroblasts” increase their output of matrix metalloproteinase enzymes which may play an active role in villus atrophy. Intraepithelial lymphocytes also increase, but their role is not clear26-29.
    Human leukocyte antigen (HLA) genes encode the class II molecules DQ2 and DQ8, the key genetic risk factors in celiac disease. The HLA system is the human version of the major histocompatibility complex (MHC). HLA class II molecules are expressed on the surface of antigen presenting cells such as dendritic cells. Virtually all celiac disease patients carry DQ2 or DQ8, but carrying DQ2 or DQ8 alone does not confer celiac disease. DQ2 and DQ8 molecules may be encoded by several different haplotypes. Haplotypes are combinations of alternative genes for the same trait (alleles) occupying different locations on a chromosome which tend to be inherited as a group. These DQ2 and DQ8 molecules play a central role in the pathogenesis of celiac disease. The function of HLA class II molecules is to bind peptide antigens and present them to CD4+ T-cell receptors. The pattern of amino acids in the makeup of the chain that forms the peptide antigen is called an epitope, and that pattern is crucial to the binding between HLA molecule and peptide. It is the misfortune of celiac disease patients that epitopes of deamidated gluten peptides just happen to match up and firmly anchor into the binding grooves of DQ2 and DQ8 molecules. This strong binding results in the activation of CD4+ T cells and the subsequent processes which damage the intestinal epithelia. But why is it that CD4+ T cells are not activated in everyone who possesses the appropriate HLA-DQ2 and -DQ8 haplotypes? The question arises again. Why is one identical twin tolerant to gluten and not the other?26-30
    Dendritic Cells
    Whether an outcome of tolerance or intolerance results when a dendritic cell presents an antigen to a naive T cell depends on many factors. A dendritic cell is a special type of white blood cell (leukocyte) which circulates throughout the body looking to acquire antigens. Dendritic cells engulf and internalize antigens through a process called endocytosis. In receptor-mediated endocytosis, dendritic cells express a variety of surface receptors to capture protein antigens. In macropinocytosis, dendritic cells surround and “drink up” soluble antigens. In phagocytosis, dendritic cells engulf pathogenic bacteria, viruses, fungi, dead or infected cells, or their products. After digestion and processing, the antigens are bound to HLA (or MHC) molecules and expressed on the surface of dendritic cells for presentation to T cells. Antigen presentation occurs after dendritic cells migrate to the lymph nodes which are rich with T cells. T cell activation also requires secondary stimulation by costimulatory molecules expressed on the dendritic cell surface. Dendritic cells have three stages in their life cycle: Precursor, immature and mature. Precursor dendritic cells arise from the bone marrow. Subsets of precursor dendritic cells have been identified that grow and differ with regard to observable characteristics (phenotype), function and anatomical location. Studies have linked dendritic cell subsets with particular functions such as T cell differentiation or tolerance induction. Immature dendritic cells spread throughout tissues seeking antigens. Dendritic cells enter the mature stage when they reach the lymph nodes after antigen capture and having become primed and ready to activate T cells with antigens and costimulatory molecules. The processing of antigens produces roughly 100,000 to 300,000 peptide-laden HLA molecules on the dendritic cell surface, most peptides represented by about 100 copies. A single mature dendritic cell is capable of stimulating 100–3,000 T cells31-34.
    Immature dendritic cells are capable of phagocytosis of bacteria. Dendritic cell phagocytosis of Salmonella and Borrelia burgdorferi has been observed and studied. Immature dendritic cells roaming the lamina propria below the epithelial cells of the intestine not only capture bacteria which invade and cross the epithelial barrier, but have been observed reaching through the tight junctions between epithelial cells with their dendrite arms to directly sample non-invasive bacteria in the gut lumen and mucosa tissues outside the epithelium34-37.
    Immature dendritic cells express a variety of surface receptors which when stimulated cause dendritic cells to mature and respond in specific ways which can result in tolerance or immune activity. These receptors include Toll-like receptors (TLR), cytokine receptors, TNF (tumor necrosis factor) receptor, immunoglobulin (antibody) receptors, and sensors for cell death. TNF and other cykotine inflammatory mediators signal infections. In particular, interleukin-1 (IL-1) can prevent oral tolerance in mice by altering the response of normally tolerogenic dendritic cells into an active immune response32,34.
    Toll-like receptors are known as pattern recognition receptors which identify structural components found only on the surface of bacteria and other pathogens. These components are referred to as pathogen-associated molecular patterns (PAMPs). At least 10 types of TLR have been identified in humans and given the designations, TLR1-TLR10. Examples of PAMP include microbial carbohydrates like the toxin lipopolysaccharides (LPS), flagellin, products from bacterial cell walls, bacterial RNA and DNA. Signaling through different TLR evokes distinct biological responses. TLR expressed differently by different dendritic cell subsets may determine the manner in which dendritic cell subsets respond to particular microbial structures34,39.
    Mature dendritic cells can produce cytokines while activating CD4+ T cells which may influence T cell differentiation and function. Activated T cells divide and proliferate and differentiate into a variety of types. Tolerance and immunity induction are influenced most by differentiation into type 1 and type 2 helper T cells (Th1 and Th2) and regulatory T cells. The type of cytokines produced by the T cells determine their classification. Th2 responses favor tolerance. Th1 responses favor immunity and inflammation. Regulatory T cells suppress immune responses. IL-10 produced by dendritic cells appears to contribute to Th2 and regulatory T cell responses. Dendritic cell production of IL-12, IL-18, and IL-23 contribute to a Th1 response34,40.
    Why Does Tolerance to Gluten Fail?
    Okay. So why does the immune system fail to tolerate gluten in celiac disease? The immune system receives and responds to all kinds of signals from a pathogen, but how can a simple gluten peptide turn this complex immune machinery into a force against itself? Thinking about this leads to a very provocative question:
    What if instead of responding to gluten peptides alone, the immune system responds to a pathogenic gut bacteria which routinely ingests gluten peptides?
    A 33 amino acid gluten peptide has been identified as the primary initiator of the inflammatory response in celiac disease. This peptide contains a number of amino acid sequences which correspond to epitopes known to activate T cells and initiate celiac disease response. In particular, this 33-mer peptide was identified because it remained intact in the residue of a solution of gliadin mixed with gastric and pancreatic enzymes. This demonstrates some gluten peptides are difficult to breakdown by normal digestive processes. Another experiment identified a 17 amino acid gluten peptide which also contained epitopes associated with celiac disease41,42.
    Bacteria do not ingest nutrients in the normal sense. Nutrients are transported across cell membranes via several different mechanisms. Transported nutrients are necessarily limited in size. Nutrients are broken down externally by enzymes and by processes such as fermentation, an oxidation process resulting from acids produced by bacteria. Growth factors consisting of purines, pyrimidines, vitamins and amino acids are required by some bacteria in order to grow. Other bacteria are able to synthesize these essential growth factors. Researchers have found that some bacteria can transport and internalize amino acids in the form of peptides. Studies so far have found peptides up to 18 amino acids in length can be internalized by bacteria43-46.
    Epitopes of gluten peptides deamidated by tissue transglutaminase (tTG) are believed central to celiac disease pathogenesis. However, a study of gluten response in children with celiac disease found that T cells can respond to native gluten peptides independent of deamidation47. Celiac disease may begin its course without deamidation. As the disease progresses, inflammation may cause an increase in expression of tTG. An increase in tTG expression has been shown during wound healing, in liver injury, and in response to an inflammatory stimulus by lipopolysaccharide48-50. Through a process called epitope spreading and with the increase in tTG expression, deamidation of gluten peptides is more likely to occur and T cell response to deamidated gluten peptides likely develops. tTG is expressed in the epithelial brush border and extracellularly in the subepithelial region26 (The brush border is composed of the microvilli found on each individual epithelial cell).
    In the course of evolution of bacteria in the gut, it would seem highly plausible that at least one or more bacteria species have evolved and adapted in some way to transport, internalize and utilize gluten peptides as a source of amino acids. Since tTG is expressed in the epithelial brush border, deamidated gluten peptides are available to such bacteria (though in the early stage of celiac disease deamidation may not be required). If these bacteria colonize the gut and exhibit some pathogenic characteristic, such as expressing lipopolysaccharide, dendritic cells may be signaled to reach through the epithelial barrier into the lumen to sample and phagocytize the bacteria. When this bacteria is digested and processed by the dendritic cells, the antigens bound to HLA molecules and expressed on the dendritic cell surface are likely to include the difficult to breakdown, intact gluten peptides that have been internalized by the bacteria. As far as the immune system is concerned, these gluten peptides are indistinguishable from the other bacterial peptides bound to HLA molecules expressed on the dendritic cell surface. When these gluten peptide antigens are bound to HLA-DQ2 or -DQ8 molecules and presented to CD4+ T cells, the T cells simultaneously receive all the signals telling them that the gluten peptide is an antigen from a pathogenic bacteria. The result is that the immune system responds to the presence of gluten as though pathogenic bacteria were present. Such gluten-ingesting bacteria may be the missing link in the pathogenesis of Celiac Disease.
    If these bacteria exist, there is now a clear explanation as to why one identical twin may develop celiac disease and not the other. Of course, the presence of such a bacteria in the gut of one twin and not the other would fully explain the discordance. It is also possible that such a bacteria may exist in both twins, but is kept under control by the mix of commensal bacteria colonizing the gut of one twin. Some disturbance to this mix, such as an infection or use of antibiotics, might provide an opportunity for this gluten-ingesting bacteria to colonize and proliferate to a level where its pathogenic properties, such as production of endotoxins, are sensed by the immune system initiating the onset of celiac disease. The existence of such bacteria could also explain why there may be varying degrees of gluten sensitivity, even in individuals without DQ2 and DQ8 molecules.
    The possibility that these gluten-ingesting bacteria may exist raises another intriguing question: If these gluten-ingesting bacteria are controlled or eliminated from the gut, could tolerance to gluten be restored? There could be a very real possibility that celiac disease might be cured by eliminating these bacteria. After all, peptic ulcers can be cured by eliminating Helicobacter pylori.
    The Future
    So where should research go from here? The most obvious path would be first to try to find and identify any gut bacteria that has gluten peptides present within its cell membranes. From there, the possible link to celiac disease could be studied. Additionally, it would be quite valuable to initiate a large long-term study of the makeup of commensal bacteria in identical twins beginning at birth via fecal samples. By comparing the differences in microflora and the onset and discordance of diseases in identical twins over many years, the relationships of specific species of bacteria to specific diseases, including celiac disease, could be established. And if it proves to be true that gluten-ingesting bacteria cause celiac disease, a similar mechanism involving bacteria and peptides from other proteins may be the root cause for many other autoimmune diseases. A whole class of autoimmune diseases might be cured by eliminating specific species of bacteria.
    Roy Jamron holds degrees in physics and engineering from the University of Michigan and the University of California at Davis and actively pursues and investigates research on celiac disease and related disorders.

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    Greco L, Romino R, Coto I, Di Cosmo N, Percopo S, Maglio M, Paparo F, Gasperi V, Limongelli MG, Cotichini R, D'Agate C, Tinto N, Sacchetti L, Tosi R, Stazi MA. The first large population based twin study of coeliac disease. Gut 2002 May;50(5):624-8. Bardella MT, Fredella C, Prampolini L, Marino R, Conte D, Giunta AM. Gluten sensitivity in monozygous twins: a long-term follow-up of five pairs. Am J Gastroenterol 2000 Jun;95(6):1503-5. Bingley PJ, Williams AJ, Norcross AJ, Unsworth DJ, Lock RJ, Ness AR, Jones RW. Undiagnosed coeliac disease at age seven: population based prospective birth cohort study. BMJ 2004 Feb 7;328(735):322-3. Sollid LM. Breast milk against coeliac disease. Gut 2002 Dec;51(6):767-8. Nash S. Does exclusive breast-feeding reduce the risk of coeliac disease in children? Br J Community Nurs 2003 Mar;8(3):127-32. Ivarsson A, Hernell O, Stenlund H, Persson LA. Breast-feeding protects against celiac disease. Am J Clin Nutr 2002 May;75(5):914-21. Peters U, Schneeweiss S, Trautwein EA, Erbersdobler HF. A case-control study of the effect of infant feeding on celiac disease. Ann Nutr Metab 2001;45(4):135-42. Stepankova R, Kofronova O, Tuckova L, Kozakova H, Cebra JJ, Tlaskalova-Hogenova H. Experimentally induced gluten enteropathy and protective effect of epidermal growth factor in artificially fed neonatal rats. J Pediatr Gastroenterol Nutr 2003 Jan;36(1):96-104. Martin R, Langa S, Reviriego C, Jiminez E, Marin ML, Xaus J, Fernandez L, Rodriguez JM. Human milk is a source of lactic acid bacteria for the infant gut. J Pediatr 2003 Dec;143(6):754-8. Goldman AS. Modulation of the gastrointestinal tract of infants by human milk. Interfaces and interactions. An evolutionary perspective. J Nutr 2000 Feb;130(2S Suppl):426S-431S. Fanaro S, Chierici R, Guerrini P, Vigi V. Intestinal microflora in early infancy: composition and development. Acta Paediatr Suppl 2003 Sep;91(441):48-55. Dunne C, O'Mahony L, Murphy L, Thornton G, Morrissey D, O'Halloran S, Feeney M, Flynn S, Fitzgerald G, Daly C, Kiely B, O'Sullivan GC, Shanahan F, Collins JK. In vitro selection criteria for probiotic bacteria of human origin: correlation with in vivo findings. Am J Clin Nutr 2001 Feb;73(2 Suppl):386S-392S. Mai V, Morris JG Jr. Colonic bacterial flora: changing understandings in the molecular age. J Nutr 2004 Feb;134(2):459-64 Gronlund MM, Arvilommi H, Kero P, Lehtonen OP, Isolauri E. Importance of intestinal colonisation in the maturation of humoral immunity in early infancy: a prospective follow up study of healthy infants aged 0-6 months. Arch Dis Child Fetal Neonatal Ed 2000 Nov;83(3):F186-92. Hooper LV, Wong MH, Thelin A, Hansson L, Falk PG, Gordon JI. Molecular analysis of commensal host-microbial relationships in the intestine. Science 2001 Feb 2;291(5505):881-4. Hooper LV, Xu J, Falk PG, Midtvedt T, Gordon JI. A molecular sensor that allows a gut commensal to control its nutrient foundation in a competitive ecosystem. Proc Natl Acad Sci U S A 1999 Aug 17;96(17):9833-8. Stappenbeck TS, Hooper LV, Gordon JI. Developmental regulation of intestinal angiogenesis by indigenous microbes via Paneth cells. Proc Natl Acad Sci U S A 2002 Nov 26;99(24):15451-5. Hooper LV, Stappenbeck TS, Hong CV, Gordon JI. Angiogenins: a new class of microbicidal proteins involved in innate immunity. Nat Immunol 2003 Mar;4(3):269-73. Lanning D, Sethupathi P, Rhee KJ, Zhai SK, Knight KL. Intestinal microflora and diversification of the rabbit antibody repertoire. J Immunol 2000 Aug 15;165(4):2012-9. Rhee KJ, Sethupathi P, Driks A, Lanning DK, Knight KL. Role of commensal bacteria in development of gut-associated lymphoid tissues and preimmune antibody repertoire. J Immunol 2004 Jan 15;172(2):1118-24. Garcia-Lafuente A, Antolin M, Guarner F, Crespo E, Malagelada JR. Modulation of colonic barrier function by the composition of the commensal flora in the rat. Gut 2001 Apr;48(4):503-7. Bai AP, Ouyang Q, Zhang W, Wang CH, Li SF. Probiotics inhibit TNF-alpha-induced interleukin-8 secretion of HT29 cells. World J Gastroenterol 2004 Feb 1;10(3):455-7. Guarner F, Malagelada JR. Gut flora in health and disease. Lancet 2003 Feb 8;361(9356):512-9. Hill MJ. Intestinal flora and endogenous vitamin synthesis. Eur J Cancer Prev 1997 Mar;6 Suppl 1:S43-5. Card T, Logan RF, Rodrigues LC, Wheeler JG. Antibiotic use and the development of Crohn's disease. Gut 2004 Feb;53(2):246-50. Sollid LM. Coeliac disease: dissecting a complex inflammatory disorder. Nat Rev Immunol 2002 Sep;2(9):647-55. Dewar D, Pereira SP, Ciclitira PJ. The pathogenesis of coeliac disease. Int J Biochem Cell Biol 2004 Jan;36(1):17-24. Farrell RJ, Kelly CP. Celiac sprue. N Engl J Med 2002 Jan 17;346(3):180-8. Daum S, Bauer U, Foss HD, Schuppan D, Stein H, Riecken EO, Ullrich R. Increased expression of mRNA for matrix metalloproteinases-1 and -3 and tissue inhibitor of metalloproteinases-1 in intestinal biopsy specimens from patients with coeliac disease. Gut 1999 Jan;44(1):17-25. Louka AS, Sollid LM. HLA in coeliac disease: unravelling the complex genetics of a complex disorder. Tissue Antigens 2003 Feb;61(2):105-17. DeMeyer ES, Baar J. Dendritic Cells: The Sentry Cells of the Immune System. Oncology Education Services, Inc. http://oes.digiton.com/dcell/ Guermonprez P, Valladeau J, Zitvogel L, Thery C, Amigorena S. Antigen presentation and T cell stimulation by dendritic cells. Annu Rev Immunol 2002;20:621-67. Klein J, Sato A. The HLA system. First of two parts. N Engl J Med 2000 Sep 7;343(10):702-9. Stagg AJ, Hart AL, Knight SC, Kamm MA. The dendritic cell: its role in intestinal inflammation and relationship with gut bacteria. Gut 2003 Oct;52(10):1522-9. Sundquist M, Rydstrom A, Wick MJ. Immunity to Salmonella from a dendritic point of view. Cell Microbiol 2004 Jan;6(1):1-11. Suhonen J, Komi J, Soukka J, Lassila O, Viljanen MK. Interaction between Borrelia burgdorferi and immature human dendritic cells. Scand J Immunol 2003 Jul;58(1):67-75. Uhlig HH, Powrie F. Dendritic cells and the intestinal bacterial flora: a role for localized mucosal immune responses. J Clin Invest 2003 Sep;112(5):648-51. Rescigno M, Urbano M, Valzasina B, Francolini M, Rotta G, Bonasio R, Granucci F, Kraehenbuhl JP, Ricciardi-Castagnoli P. Dendritic cells express tight junction proteins and penetrate gut epithelial monolayers to sample bacteria. Nat Immunol 2001 Apr;2(4):361-7. Singh BP, Chauhan RS, Singhal LK. Toll-like receptors and their role in innate immunity. Current Science 2003 Oct;85(8):1156-1164. Mowat AM. Anatomical basis of tolerance and immunity to intestinal antigens. Nat Rev Immunol 2003 Apr;3(4):331-41. Shan L, Molberg O, Parrot I, Hausch F, Filiz F, Gray GM, Sollid LM, Khosla C. Structural basis for gluten intolerance in celiac sprue. Science 2002 Sep 27;297(5590):2275-9. Anderson RP, Degano P, Godkin AJ, Jewell DP, Hill AV. In vivo antigen challenge in celiac disease identifies a single transglutaminase-modified peptide as the dominant A-gliadin T-cell epitope. Nat Med 2000 Mar;6(3):337-42. Todar K. Todar's Online Textbook of Bacteriology. Univ of Wisconsin Department of Bacteriology. http://www.textbookofbacteriology.net Monnet V. Bacterial oligopeptide-binding proteins. Cell Mol Life Sci 2003 Oct;60(10):2100-14. Foucaud C, Hemme D, Desmazeaud M. Peptide utilization by Lactococcus lactis and Leuconostoc mesenteroides. Lett Appl Microbiol 2001 Jan;32(1):20-5. Detmers FJ, Kunji ER, Lanfermeijer FC, Poolman B, Konings WN. Kinetics and specificity of peptide uptake by the oligopeptide transport system of Lactococcus lactis. Biochemistry 1998 Nov 24;37(47):16671-9. Vader W, Kooy Y, Van Veelen P, De Ru A, Harris D, Benckhuijsen W, Pena S, Mearin L, Drijfhout JW, Koning F. The gluten response in children with celiac disease is directed toward multiple gliadin and glutenin peptides. Gastroenterology 2002 Jun;122(7):1729-37. Haroon ZA, Hettasch JM, Lai TS, Dewhirst MW, Greenberg CS. Tissue transglutaminase is expressed, active, and directly involved in rat dermal wound healing and angiogenesis. FASEB J 1999 Oct;13(13):1787-95. Nardacci R, Lo Iacono O, Ciccosanti F, Falasca L, Addesso M, Amendola A, Antonucci G, Craxi A, Fimia GM, Iadevaia V, Melino G, Ruco L, Tocci G, Ippolito G, Piacentini M. Transglutaminase type II plays a protective role in hepatic injury. Am J Pathol 2003 Apr;162(4):1293-303. Bowness JM, Tarr AH. Increase in transglutaminase and its extracellular products in response to an inflammatory stimulus by lipopolysaccharide. Mol Cell Biochem 1997 Apr;169(1-2):157-63.

    Jefferson Adams
    Celiac.com 04/07/2008 - No, this is not some kind of April Fool’s joke.When I read this report, I just about fell off my chair. New research indicates thatbeing poor and living in squalor might actually provide some benefitagainst the development of celiac disease.
    A team of medicalresearchers recently set out to examine gene-environmental interactionsin the pathogenesis of celiac disease. The research team was made up ofA. Kondrashova, K. Mustalahti, K. Kaukinen, H. Viskari, V. Volodicheva,A. M. Haapala, J. Ilonen, M. Knip, M. Mäki, H. Hyöty, T. E. Group.Finland and nearby Russian Karelia have populations that eat about thesame amounts of the same grains and grain products. The two populationsalso have a high degree of shared genetic ancestry. The only majordifference between the populations of the two areas lies in theirsocioeconomic conditions.
    The region of Russian Karelia ismuch poorer than the neighboring areas in nearby Finland. Thesanitation levels in Russian Karelia are also distinctly inferior thanthey are in Finland. The researchers compared the prevalence of celiacdisease and predisposing human leukocyte antigen (HLA) alleles inpopulations from Russian Karelia and Finland. The team performedscreening for tissue transglutaminase antibodies (tTG) and HLA-DQalleles on 1988 school-age children from Karelia and 3654 children fromFinland. Children with transglutaminase antibodies were encouraged tohave a duodenal biopsy.
    Interestingly, the patients fromRussian Karelia showed tTG antibodies far less often than their Finnishcounterparts (0.6% compared to 1.4%, P = 0.005). The patients fromRussian Karelia also showed Immunoglobulin class G (IgG) antigliadinantibodies far less frequently than their Finnish patients (10.2%compared to 28.3%, P<0.0001).
    The researchers confirmed adiagnosis of celiac disease by duodenal biopsy in four of the eighttransglutaminase antibody-positive Karelian children, for an occurrencerate of 1 in 496 versus 1 in 107 Finnish children.
    In bothgroups, the same HLA-DQ alleles were associated with celiac disease andthe presence of transglutaminase antibodies. The patients from RussianKarelia showed a much lower prevalence of transglutaminase antibodiesand celiac disease than the Finnish children. 
    The poorconditions and inferior hygienic conditions in Russian Karelia mightprovide some kind of protection against the development of celiacdisease. The value of studies like this aren’t to make us wax nostalgicfor poverty, or to encourage people to fend off celiac disease bybecoming poor and living in squalid conditions. The value of a studylike this lies in the idea that there may be more to the development ofceliac disease than simple biological factors. That environmentalconditions might play a key role in both the frequency ofceliac-related antibodies, and in the development of the disease itselfis quite intriguing and clearly warrants further and more comprehensivestudy.
    Ann Med. 2008;40(3):223-31.


    Jefferson Adams
    Celiac.com 05/02/2012 - Doctors and researchers are still debating the usefulness of active blood screening for spotting celiac disease in older populations. Studies do suggest that many cases of celiac disease go undetected, especially in the older population. One unanswered question is whether screening does any good for older people who have been eating gluten many decades.
    A team of researchers recently studied the clinical benefit of a gluten-free diet in screen-detected older celiac disease patients. The research team included Anitta Vilppula, Katri Kaukinen, Liisa Luostarinen, Ilkka Krekelä, Heikki Patrikainen, Raisa Valve, Markku Luostarinen, Kaija Laurila, Markku Mäki, and Pekka Collin.
    They are affiliated with the Department of Neurology, the Department of Internal Medicine and the Department of Surgery at Päijät-Häme Central Hospital, and the University of Helsinki's Department of Education and Development in Lahti, Finland, the Department of Gastroenterology and Alimentary Tract Surgery the School of Medicine, and the Paediatric Research Centre at the University of Tampere and Tampere University Hospital, Tampere, Finland.
    For their study, the researchers evaluated the benefit of active detection and implementation of a gluten-free diet in elder populations with for celiac disease.
    The team evaluated thirty-five biopsy-proven celiac patients over 50 years of age, each of whom had celiac disease detected by mass blood screening.
    They looked at bone mineral density, dietary compliance, disease history, quality of life, and symptoms at baseline and after 1-2 years of a gluten-free diet. They also looked at small bowel biopsy, serology, laboratory parameters assessing malabsorption, and bone mineral density.
    Using surveys, the team established gastrointestinal symptom ratings and quality of life by psychological general well-being. The used this information to rate symptoms.
    They found patient dietary compliance to be good overall.  Initial tests on the patients showed reduced serum ferritin levels, pointing to subclinical iron deficiency. This trend reversed after patients followed a gluten-free diet.
    Initially low vitamin B12, vitamin D and erythrocyte folic acid levels increased significantly on a gluten-free diet.
    Patient histories showed that those with celiac disease had sustained more low-energy fractures, and sustained such fractures more frequently than the general population. A gluten-free diet brings with it a beneficial increase in bone mineral density.
    The team also noticed that many gastrointestinal symptoms disappeared, even though though many patients reported only subtle symptoms upon diagnosis.
    Quality of life remained unchanged. According to the study team, two out of three patients would have been diagnosed even without screening if the family history, fractures or concomitant autoimmune diseases had been factored in.
    Results showed that patients who had celiac disease detected by mass blood screen did, in fact, benefit from a gluten-free diet. For doctors evaluating older patients, the team advocates a high index of suspicion and active case-finding in celiac disease as an alternative to mass screening.
    Source:
    BMC Gastroenterology 2011, 11:136. doi:10.1186/1471-230X-11-136

    Jefferson Adams
    Celiac.com 04/22/2014 - Blood tests are highly valuable for diagnosing celiac disease. However, their role in gauging mucosal healing in celiac children who have adopted gluten-free diets is unclear.
    A team of researchers recently set out to compare the performance of antibody tests in predicting small-intestinal mucosal status in diagnosis and follow-up of pediatric celiac disease.
    The research team included Edith Vécsei, Stephanie Steinwendner, Hubert Kogler, Albina Innerhofer, Karin Hammer, Oskar A Haas, Gabriele Amann, Andreas Chott, Harald Vogelsang, Regine Schoenlechner, Wolfgang Huf, and Andreas Vécsei.
    They are variously affiliated with the Clinical Department of Pathology and the Department of Internal Medicine III of the Division for Gastroenterology and Hepatology, the Center for Medical Physics and Biomedical Engineering, the Department of Pediatrics and Pediatric Gastroenterology of St. Anna Children's Hospital, all at Medical University Vienna, and with the Institute of Pathology and Microbiology, Wilhelminenspital in Vienna, and with the Department of Food Science and Technology, Institute of Food Technology, University of Natural Resources and Life Sciences in Vienna, Austria.
    The team conducted a prospective cohort study at a tertiary-care center, where 148 children received biopsies either for symptoms ± positive celiac disease antibodies (group A; n = 95) or following up celiac disease diagnosed ≥ 1 year before study enrollment (group B; n = 53).
    Using biopsy (Marsh ≥ 2) as the criterion standard, they calculated areas under ROC curves (AUCs) and likelihood-ratios to gauge the performance of antibody tests against tissue transglutaminase (TG2), deamidated gliadin peptide (DGP) and endomysium (EMA).
    They found that AUC values were higher when tests were used for celiac disease diagnosis compared with follow-up: 1 vs. 0.86 (P = 0.100) for TG2-IgA, 0.85 vs. 0.74 (P = 0.421) for TG2-IgG, 0.97 vs. 0.61 (P = 0.004) for DPG-IgA, and 0.99 vs. 0.88 (P = 0.053) for DPG-IgG, respectively.
    Empirical power was 85% for the DPG-IgA comparison, and on average 33% (range 13–43) for the non-significant comparisons. A total of 88.7% of group B children showed mucosal healing, at an average of 2.2 years after primary diagnosis.
    Only the negative likelihood-ratio of EMA was low enough (0.097) to effectively rule out persistent mucosal injury. However, out of 12 EMA-positive children with mucosal healing, 9 subsequently tested EMA-negative.
    Among the celiac disease antibodies examined, negative EMA most reliably predict mucosal healing. In general, however, antibody tests, especially DPG-IgA, are of limited value in predicting the mucosal status in the early years after celiac diagnosis, though they may do better over a longer time.
    Source:
    BMC Gastroenterology 2014, 14:28. doi:10.1186/1471-230X-14-28

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    Bakery On Main started in the small bakery of a natural foods market on Main Street in Glastonbury, Connecticut. Founder Michael Smulders listened when his customers with Celiac Disease would mention the lack of good tasting, gluten-free options available to them. Upon learning this, he believed that nobody should have to suffer due to any kind of food allergy or dietary need. From then on, his mission became creating delicious and fearlessly unique gluten-free products that were clean and great tasting, while still being safe for his Celiac customers!
    Premium ingredients, bakeshop delicious recipes, and happy customers were our inspiration from the beginning— and are still the cornerstones of Bakery On Main today. We are a fiercely ethical company that believes in integrity and feels that happiness and wholesome, great tasting food should be harmonious. We strive for that in everything we bake in our dedicated gluten-free facility that is GFCO Certified and SQF Level 3 Certified. We use only natural, NON-GMO Project Verified ingredients and all of our products are certified Kosher Parve, dairy and casein free, and we have recently introduced certified Organic items as well! 
    Our passion is to bake the very best products while bringing happiness to our customers, each other, and all those we meet!
    We are available during normal business hours at: 1-888-533-8118 EST.
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    Jefferson Adams
    Celiac.com 06/20/2018 - Currently, the only way to manage celiac disease is to eliminate gluten from the diet. That could be set to change as clinical trials begin in Australia for a new vaccine that aims to switch off the immune response to gluten. 
    The trials are set to begin at Australia’s University of the Sunshine Coast Clinical Trials Centre. The vaccine is designed to allow people with celiac disease to consume gluten with no adverse effects. A successful vaccine could be the beginning of the end for the gluten-free diet as the only currently viable treatment for celiac disease. That could be a massive breakthrough for people with celiac disease.
    USC’s Clinical Trials Centre Director Lucas Litewka said trial participants would receive an injection of the vaccine twice a week for seven weeks. The trials will be conducted alongside gastroenterologist Dr. James Daveson, who called the vaccine “a very exciting potential new therapy that has been undergoing clinical trials for several years now.”
    Dr. Daveson said the investigational vaccine might potentially restore gluten tolerance to people with celiac disease.The trial is open to adults between the ages of 18 and 70 who have clinically diagnosed celiac disease, and have followed a strict gluten-free diet for at least 12 months. Anyone interested in participating can go to www.joinourtrials.com.
    Read more at the website for Australia’s University of the Sunshine Coast Clinical Trials Centre.

    Source:
    FoodProcessing.com.au

    Jefferson Adams
    Celiac.com 06/19/2018 - Could baking soda help reduce the inflammation and damage caused by autoimmune diseases like rheumatoid arthritis, and celiac disease? Scientists at the Medical College of Georgia at Augusta University say that a daily dose of baking soda may in fact help reduce inflammation and damage caused by autoimmune diseases like rheumatoid arthritis, and celiac disease.
    Those scientists recently gathered some of the first evidence to show that cheap, over-the-counter antacids can prompt the spleen to promote an anti-inflammatory environment that could be helpful in combating inflammatory disease.
    A type of cell called mesothelial cells line our body cavities, like the digestive tract. They have little fingers, called microvilli, that sense the environment, and warn the organs they cover that there is an invader and an immune response is needed.
    The team’s data shows that when rats or healthy people drink a solution of baking soda, the stomach makes more acid, which causes mesothelial cells on the outside of the spleen to tell the spleen to go easy on the immune response.  "It's most likely a hamburger not a bacterial infection," is basically the message, says Dr. Paul O'Connor, renal physiologist in the MCG Department of Physiology at Augusta University and the study's corresponding author.
    That message, which is transmitted with help from a chemical messenger called acetylcholine, seems to encourage the gut to shift against inflammation, say the scientists.
    In patients who drank water with baking soda for two weeks, immune cells called macrophages, shifted from primarily those that promote inflammation, called M1, to those that reduce it, called M2. "The shift from inflammatory to an anti-inflammatory profile is happening everywhere," O'Connor says. "We saw it in the kidneys, we saw it in the spleen, now we see it in the peripheral blood."
    O'Connor hopes drinking baking soda can one day produce similar results for people with autoimmune disease. "You are not really turning anything off or on, you are just pushing it toward one side by giving an anti-inflammatory stimulus," he says, in this case, away from harmful inflammation. "It's potentially a really safe way to treat inflammatory disease."
    The research was funded by the National Institutes of Health.
    Read more at: Sciencedaily.com

    Jefferson Adams
    Celiac.com 06/18/2018 - Celiac disease has been mainly associated with Caucasian populations in Northern Europe, and their descendants in other countries, but new scientific evidence is beginning to challenge that view. Still, the exact global prevalence of celiac disease remains unknown.  To get better data on that issue, a team of researchers recently conducted a comprehensive review and meta-analysis to get a reasonably accurate estimate the global prevalence of celiac disease. 
    The research team included P Singh, A Arora, TA Strand, DA Leffler, C Catassi, PH Green, CP Kelly, V Ahuja, and GK Makharia. They are variously affiliated with the Division of Gastroenterology and Hepatology, Beth Israel Deaconess Medical Center, Boston, Massachusetts; Lady Hardinge Medical College, New Delhi, India; Innlandet Hospital Trust, Lillehammer, Norway; Centre for International Health, University of Bergen, Bergen, Norway; Division of Gastroenterology and Hepatology, Beth Israel Deaconess Medical Center, Boston, Massachusetts; Gastroenterology Research and Development, Takeda Pharmaceuticals Inc, Cambridge, MA; Department of Pediatrics, Università Politecnica delle Marche, Ancona, Italy; Department of Medicine, Columbia University Medical Center, New York, New York; USA Celiac Disease Center, Columbia University Medical Center, New York, New York; and the Department of Gastroenterology and Human Nutrition, All India Institute of Medical Sciences, New Delhi, India.
    For their review, the team searched Medline, PubMed, and EMBASE for the keywords ‘celiac disease,’ ‘celiac,’ ‘tissue transglutaminase antibody,’ ‘anti-endomysium antibody,’ ‘endomysial antibody,’ and ‘prevalence’ for studies published from January 1991 through March 2016. 
    The team cross-referenced each article with the words ‘Asia,’ ‘Europe,’ ‘Africa,’ ‘South America,’ ‘North America,’ and ‘Australia.’ They defined celiac diagnosis based on European Society of Pediatric Gastroenterology, Hepatology, and Nutrition guidelines. The team used 96 articles of 3,843 articles in their final analysis.
    Overall global prevalence of celiac disease was 1.4% in 275,818 individuals, based on positive blood tests for anti-tissue transglutaminase and/or anti-endomysial antibodies. The pooled global prevalence of biopsy-confirmed celiac disease was 0.7% in 138,792 individuals. That means that numerous people with celiac disease potentially remain undiagnosed.
    Rates of celiac disease were 0.4% in South America, 0.5% in Africa and North America, 0.6% in Asia, and 0.8% in Europe and Oceania; the prevalence was 0.6% in female vs 0.4% males. Celiac disease was significantly more common in children than adults.
    This systematic review and meta-analysis showed celiac disease to be reported worldwide. Blood test data shows celiac disease rate of 1.4%, while biopsy data shows 0.7%. The prevalence of celiac disease varies with sex, age, and location. 
    This review demonstrates a need for more comprehensive population-based studies of celiac disease in numerous countries.  The 1.4% rate indicates that there are 91.2 million people worldwide with celiac disease, and 3.9 million are in the U.S.A.
    Source:
    Clin Gastroenterol Hepatol. 2018 Jun;16(6):823-836.e2. doi: 10.1016/j.cgh.2017.06.037.

    Jefferson Adams
    Celiac.com 06/16/2018 - Summer is the time for chips and salsa. This fresh salsa recipe relies on cabbage, yes, cabbage, as a secret ingredient. The cabbage brings a delicious flavor and helps the salsa hold together nicely for scooping with your favorite chips. The result is a fresh, tasty salsa that goes great with guacamole.
    Ingredients:
    3 cups ripe fresh tomatoes, diced 1 cup shredded green cabbage ½ cup diced yellow onion ¼ cup chopped fresh cilantro 1 jalapeno, seeded 1 Serrano pepper, seeded 2 tablespoons lemon juice 2 tablespoons red wine vinegar 2 garlic cloves, minced salt to taste black pepper, to taste Directions:
    Purée all ingredients together in a blender.
    Cover and refrigerate for at least 1 hour. 
    Adjust seasoning with salt and pepper, as desired. 
    Serve is a bowl with tortilla chips and guacamole.