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  • Kristina Campbell
    Kristina Campbell

    Study Finds Gut Bacteria can Affect Intestines' Protective Layer

    Caption: New research could lead to treatment for celiac disease.

    Celiac.com 03/15/2011 - For celiacs, it's not really the cinnamon bun that's the enemy. Nor the pizza crust, nor the ravioli. It's the gliadin in these foods - the alcohol-soluble portion of the gluten protein - that's the real culprit.

    Gliadin is the "gladiator" of the human digestive tract. When we ingest gliadin, enzymes try to break it down into a form that can be absorbed by the small intestine. But gliadin resists, fighting hard to remain intact.

    A regular small intestine has, like any good fortress, a protective wall: the mucosal lining of the intestine. This layer of mucus normally acts as a barrier against gliadin's assaults. But in a celiac intestine, the mucosal lining is permeable. With gliadin's destructive power enhanced by its enzyme sidekick, tissue Transglutaminase (tTG), it quickly gets past this poorly-guarded layer.

    Scientists are working to put their finger on exactly what makes the mucosal lining of a celiac's small intestine so permeable.

    Now a January study by Czech researchers found at least one thing that affects the permeability of the intestinal mucosa: gut bacteria.

    In this study, called "Role of Intestinal Bacteria in Gliadin-Induced Changes in Intestinal Mucosa: Study in Germ-Free Rats", researchers tied off sections of rats' intestines and introduced various kinds of bacteria to each section. They wanted to measure the effect that these bacteria had on the intestinal mucus - or more specifically, on the goblet cells that produce the intestinal mucus. To ensure that the kinds of bacteria in the rats' intestines were under experimental control, the rats had been raised from birth in germ-free conditions.

    They found that introducing gliadin to the intestines had the effect of decreasing the mucus-producing cells, thereby eroding the intestines' protective layer. No big surprises there - gliadin is a fighter, a digestive "gladiator", after all.

    But when they added strains of so-called harmful bacteria, Escherichia coli (otherwise known as E coli) or Shigella, the mucus-producing cells decreased even more. The cells first secreted massive amounts of mucus, then promptly exhausted themselves and gave up. This left the intestine looking very similar to that of a person in the early stages of celiac disease, say the researchers.

    But the tale did indeed have a happy ending. Along came the good bacteria, Bifidobacterium bifidum (or "Biff" for short). The mucus-producing cells in the small intestine increased when Biff was present. In fact, Biff was able to partially reverse the mucus-decreasing effects of E coli and Shigella.

    The researchers concluded that the composition of gut bacteria has an effect on the protective mucus of the intestines: an overgrowth of bad bacteria decreases the protective layer, while the addition of good bacteria increases the protective layer. Their study may eventually lead to treatment options for human celiacs, by finding ways to protect tender intestines from the harmful effects of gliadin.

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  • About Me

    Kristina Jane Campbell is a health and education writer living in Vancouver, Canada. She blogs about intestinal health at: http://intestinalgardener.blogspot.com

  • Related Articles

    Scott Adams
    The following is from a talk given at the Gluten Intolerance Group Annual Educational Seminar on April 1, 1995 by Dr. Alessio Fasano, Pediatric Gastroenterologist, University of Maryland School of Medicine which was also reported in the May 1995 issue of the GIG Newsletter. The findings of these experts indicate that the incidence of celiac disease in the general population could be as high as 1 in 300-500 people when one takes into account all forms of the disease. Here is a report of the meeting:
    The question which was brought up was How prevalent is celiac disease?. Although there is much data on the incidence of celiac disease that has been collected in Europe, there is almost no data from the United States. After compiling data on the incidence of celiac disease in Europe, something very unusual was noticed.
    Two cities in Europe - Malmo, Sweden and Copenhagen, Denmark, which lie only 20 miles apart, seem to have a large difference in the incidence of celiac disease. In Malmo, the incidence was 1 in 500 people, which is quite high, while in Copenhagen it was 1 out of 11,000, which is much lower. Keep in mind that these figures represent only those patients whose celiac disease had been clinically diagnosed by a small intestinal biopsy.
    There are three major ways in which celiac disease presents itself in patients. The first are the asymptomatic patients who have no symptoms whatsoever, but exhibit damage to their small intestines upon examination. The second are patients with the latent form which means they have blood-tested positive for celiac disease, nut no tissue damage has occurred yet. This form will later develop into the typical or atypical forms. The third is the typical presentation, which shows up when the patient is between 6 and 18 months old. These patients develop the classic symptoms: diarrhea, fatty stools, lack of weight gain, irritability and anorexia. Typical presentations of celiac disease are rather rare in comparison to the other forms, which leads to the overall under-diagnosis of celiac disease, and is illustrated by the following statistics:
    Clinical Presentation
    Cumulative Prevalence
    Classical (Typical) Form
    1 in 2500
    Atypical - Late Onset Form 1 in 1500 Asymptomatic Form 1 in 1000 Latent Form (celiac disease Associated with other Diseases) 1 in 300-500* *Researchers in Italy have reached the conclusion that the incidence of celiac disease would be more like 1 person with celiac sprue for every 300 to 500 in the general population, when looking at all forms of the disease.
    Serological screening using anti-gliadin and anti-endomysial antibodies allows doctors to obtain a much more accurate picture of the actual number of people affected by celiac disease. In Europe, for example, researchers have found a much higher incidence of celiac disease than expected (1 in 300!), and it is spread uniformly throughout the population. Researchers re-tested the cities of Malmo and Copenhagen and found the incidence in Copenhagen to be 1 in 300. The difference between the two cities is in the clinical presentation of the disease. In Denmark there were more people who exhibited symptoms of osteoporosis, dermatitis herpetiformis, short stature and other atypical presentations. The awareness of physicians that these presentations could be celiac disease was very low.
    The discussion then turned to the United States:
    The next question discussed at the meeting was: What is the true incidence of celiac disease in the United States? The researchers believe that the recently discovered antibody markers will help in answering this question. According to them, we should soon be able to tell whether the low estimates for celiac disease in the US are fact, or if atypical presentations of celiac disease have been overlooked, thus resulting in the extraordinary low level of diagnosed celiacs. A study conducted at the University of Maryland looked at 159 children with atypical symptoms (short stature, poor weight gain, chronic diarrhea, abdominal pain, asymptomatic relatives of celiacs).
    The following chart summarizes the study:
    Study: 159 Children With Atypical Symptoms*
    Symptom Group No. Screened Positive Screen Negative Screen Short stature 78 7 71 Poor weight gain 21 6 15 Chronic diarrhea 17 1 16 Abdominal Pain 8 1 7 Asymptomatic 35 2 33 *Please keep in mind that this study was not based on a random cross-section of the population, but, rather on children who already exhibited atypical symptoms.
    It is crucial to make the correct diagnosis, and to keep even asymptomatic people free of gluten . This is due to the associated morbidity, such as chronic ill health. With regard to the pediatric population, permanent stunted growth may result from a misdiagnosis. If the physicians fail to make a timely diagnosis, there is no time for catch-up growth, and the individual may be short forever. The same is true with skeletal disorders such as osteoporosis. Everyone with celiac sprue who experiences osteoporosis must place a certain amount of blame on the physician for not diagnosing celiac disease in time to prevent such demineralization.

    Jefferson Adams
    Celiac.com 05/11/2012 - Horses are susceptible to inflammatory small bowel disease, and the condition effects horses in much the same way as it effects humans.
    As with its human counterpart, equine inflammatory small bowel disease (ISBD) is an idiopathic pathologic condition that seems to be growing more and more common.
    A research team recently conducted a study to examine the possibility that gluten may play a role in equine ISBD.
    The researchers were J.H. van der Kolk, L.A. van Putten, C.J. Mulder, G.C. Grinwis, M. Reijm, C.M. Butler, B.M. von Blomberg of the Department of Equine Sciences, Medicine Section, Faculty of Veterinary Medicine at the University of Utrecht, in Utrecht, in the Netherlands.
    For their study, the team assessed antibodies that are known to be important in the diagnosis of human celiac disease: IgA antibodies to human recombinant and guinea pig tissue-transglutaminase (TGA), native gliadin (AGA), deamidated-gliadin-peptides (DGPA), and primate and equine endomysium (EMA).
    The team measured these antibodies using blood samples from three different groups of horses: Twelve ISBD affected horses on a gluten-rich diet, along with two control groups.
    The first control group included 22 horses on a gluten-rich diet, and the second included 25 horses on a gluten-poor diet.
    The researchers measured differences (p < 0.05) in the groups using the Wilcoxon test.
    They found that both ISBD-affected horses and gluten-rich control group had significantly (p < 0.0004) higher hrTGA titers than gluten-poor control group.
    However, ISBD horses did not show significantly higher levels of any of the celiac disease related antibodies when compared to gluten-rich controls.
    Still, They found significantly higher antibody levels (TGA, EMA and DGPA) in one of the ISBD horses.
    They put that horse, 14-year-old stallion, on a gluten-free ration for 6 months. They then reassessed his antibodies and found a significant reduction of antibody levels, along with clinical recovery associated with improved duodenal histopathology.
    The researchers write that this is the first such study assessing gluten-related antibodies in horses and that the results suggest a potential pathogenic role of gluten in at least some cases of equine ISBD.
    These clinical results suggest that further study into the immunologic basis of possible gluten-sensitive enteropathy in horses might have important implications for the human manifestation of the disease.
    Source:
    Vet Q. 2012 Apr 10.

    Jefferson Adams
    Celiac.com 08/23/2013 - Previous studies have noted the presence of dental enamel defects in people with celiac disease.
    A team of researchers recently set out to study the prevalence of dental enamel defects in adults with celiac disease, and to determine if there is in fact a connection between the grade of teeth lesion and clinical parameters present at the time of diagnosis of celiac disease.
    The research team included L.Trotta, F. Biagi, P.I. Bianchi, A. Marchese, C. Vattiato, D. Balduzzi, V. Collesano, and G.R. Corazza.
    They are affiliated with the Coeliac Centre/First Department of Internal Medicine at the Fondazione IRCCS Policlinico San Matteo at the University of Pavia in Italy.
    The team looked at 54 celiac disease patients who had undergone dental examination. The patients included 41 females and 13 males, with an average age of 37±13 years, and with an average age of 31±14years at the time of diagnosis.
    Symptoms leading to diagnosis were diarrhea/weight loss (32 pts.), anaemia (19 pts.), familiarity (3 pts.). None of the patients was diagnosed because of enamel defects.
    At the time of evaluation, all of the patients were following a gluten-free diet.
    The team classified enamel defects from grade 0 to 4 according to severity. They found dental enamel defects in 46 of the 54 patients (85.2%). They found grade 1 defects in 18 patients (33.3%), grade 2 defects in 16 patients (29.6%), grade 3 defects in 8 patients (14.8%), and grade 4 defects in 4 patients (7.4%).
    They also observed that grades 3 and 4 were more common in patients diagnosed with classical rather than non-classical coeliac disease (10/32 vs. 2/20). However, this was not statistically significant.
    From this study, the team concludes that enamel defects are common in adult celiac disease, and that the observation of enamel defects offers a way to diagnose celiac disease.
    Source:
     Eur J Intern Med. 2013 Apr 6. pii: S0953-6205(13)00091-5. doi: 10.1016/j.ejim.2013.03.007. [Epub ahead of print]

    Jefferson Adams
    Celiac.com 03/24/2014 - Two new studies have confirmed colonization of gluten-degrading bacteria in the human mouth and in the upper gastrointestinal tracts respectively.
    Both studies come out of the Department of Periodontology and Oral Biology, Boston University Henry M. Goldman School of Dental Medicine in Boston, Massachusetts. The research teams included Maram Zamakhchari, Guoxian Wei, Floyd Dewhirst, Jaeseop Lee, Detlef Schuppan, Frank G. Oppenheim, and Eva J. Helmerhorst.
    Gluten is notoriously hard for mammals to digest, because gliadin proteins resist mammalian proteolytic enzymes in the gut, so researchers wanted to find sources of gluten-digesting microbial enzymes from the upper gastro-intestinal tract. These microbial enzymes have the potential to neutralize the gluten peptides that act as celiac disease triggers.
    In the first study the researchers assessed proteolytic activity in suspended dental plaque towards a) gliadin-derived paranitroanilide(pNA)-linked synthetic enzyme substrates a mixture of natural gliadins and c) synthetic highly immunogenic gliadin peptides (33-mer of α2-gliadin and 26-mer of γ-gliadin).
    In addition, they conducted gliadin zymography to establish the approximate molecular weights and pH activity profiles of the gliadin-degrading oral enzymes and performed liquid iso-electric focusing to determine overall enzyme iso-electric points.
    Their results provide the first known evidence of gluten-degrading microorganisms associated with the upper gastro-intestinal tract.
    Such microorganisms may play a hitherto unappreciated role in the digestion of dietary gluten and thus protection from celiac disease in subjects at risk.
    In the second study, the team employed a selective plating strategy using gluten agar to obtain oral microorganisms with gluten-degrading capacity. They then used16S rDNA gene sequencing to carry out microbial speciations.
    To determine enzyme activity, they used gliadin-derived enzymatic substrates, gliadins in solution, gliadin zymography, and 33-mer a-gliadin and 26-mer c-gliadin immunogenic peptides.
    They separated fragments of the gliadin peptides by RP-HPLC, and structurally characterized them using mass spectrometry. They found that strains Rothia mucilaginosa and Rothia aeria showed high gluten-degrading activity. For example, gliadins (250 mg/ml) added to Rothia cell suspensions (OD620 1.2) degraded by 50% after 30 minutes of incubation.
    Importantly, the 33-mer and 26-mer immunogenic peptides were also cleaved, primarily C-terminal to Xaa-Pro-Gln (XPQ) and Xaa-Pro-Tyr (XPY). The major gliadin-degrading enzymes produced by the Rothia strains were 70–75 kDa in size, and the enzyme expressed by Rothia aeria was active over a wide pH range (pH 3–10).
    While the human digestive enzyme system lacks the capacity to cleave immunogenic gluten, such activities are naturally present in the oral microbial enzyme repertoire.
    Taken together, these studies suggest a potential for these bacteria to fuel the development of compounds that can degrade of harmful gluten peptides that trigger celiac disease in susceptible individuals.
    Source:
    PLoS One. 2011;6(9):e24455. doi: 10.1371/journal.pone.0024455. http://www.ncbi.nlm.nih.gov/pubmed/20948997

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