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Jefferson Adams posted an article in Celiac Disease & Gluten Intolerance ResearchCeliac.com 04/28/2016 - The development of celiac disease has been tied to polymorphisms in the regulator of G-protein signaling 1 (RGS1) and interleukin-12 A (IL12A) genes, but existing data are unclear and contradictory. A research team recently set out to examine the associations of two single-nucleotide polymorphisms (SNPs) (rs2816316 in RGS1 and rs17810546 in IL12A) with celiac disease risk using meta-analysis. The research team included Cong-Cong Guo, Man Wang, Feng-Di Cao, Wei-Huang Huang, Di Xiao, Xing-Guang Ye, Mei-Ling Ou, Na Zhang, Bao-Huan Zhang, Yang Liu, Guang Yang, and Chun-Xia Jing. They are variously affiliate with the Department of Epidemiology, School of Medicine, Jinan University, Guangzhou, the Department of Stomatology of the First Affiliated Hospital of Jinan University, Guangzhou, the Department of Parasitology, School of Medicine, Jinan University, Guangzhou, and the Key Laboratory of Environmental Exposure and Health in Guangzhou, Jinan University, Guangzhou, China. The team began by searching PubMed and Web of Science for RGS1 rs2816316 and IL12A rs17810546 with celiac disease risk. They then estimated the odds ratio (OR) and 95% confidence interval (CI) of each SNP. They retrieved a total of seven studies, and used Stata 12.0 to perform statistical analyses. The available data indicated the minor allele C of rs2816316 was negatively associated with celiac disease (C vs. A: OR = 0.77, 95% CI = 0.74–0.80), while they did find a positive association for the minor allele G of rs17810546 (G vs. A: OR = 1.37, 95% CI = 1.31–1.43). They found that the co-dominant model of genotype effect confirmed the significant associations between RGS1 rs2816316/IL12A rs17810546 and celiac disease. They found no evidence of any publication bias. The team's meta-analysis indicates a connection between RGS1 and IL12A and celiac disease, and provides a strong support for deeper study into the roles of RGS1 and IL12A in the development of celiac disease. Source: Int. J. Mol. Sci. 2016, 17(4), 457; doi:10.3390/ijms17040457
Jefferson Adams posted an article in Crohn's Disease and Celiac DiseaseCeliac.com 02/18/2011 - In their search for a deeper understanding of the connections between celiac disease and Crohn’s disease, scientists have begun to focus on genetic variants that trigger inflammation in the gut. A research team examining associations between celiac disease and Crohn’s disease has now confirmed four common genetic variations between the two diseases. Their discovery may help to explain why people with celiac disease suffer Crohn’s disease at higher rates than the general population. Better understanding the genetic connections will likely pave the way for new treatments for symptoms common to both conditions, such as inflammation. The study used a new method of analysis called a genome-wide association study, or GWAS. This allows researchers to look at hundreds of thousands of genetic variations, called single nucleotide polymorphisms, or SNPs, that may be involved in any one disease. The research team compared 471,504 SNPs, representing the genomes of about 10,000 people, some of whom had Crohn’s disease, some of whom had celiac disease, and others who were healthy. They found four genes that seemed to raise the risk for both diseases. Two of these genes, IL18RAP and PTPN2, had already been associated with each disease. Another, called TAGAP, had previously been identified as a risk factor in celiac disease, but was newly associated with Crohn’s disease. The fourth gene, PUS10, had been previously been tied to Crohn’s disease, celiac disease, and ulcerative colitis. Three of the four genes seem to influence immune system response to perceived threats. “The first three we can say are involved in T-lymphocyte function,” Rioux says. “They seem to have a role to play in how these cells respond to a given stimulus.” In celiac disease, gluten-induced intestinal inflammation causes damage that prevents the intestine from absorbing nutrients in food. This can cause a wide range of problems, from anemia to osteoporosis to lactose intolerance. In Crohn’s disease, inflammation of the digestive tract often causes the bowel to empty frequently, resulting in diarrhea, among other problems. Some research shows that people with one condition are more likely to have the other. One study, for example, found that more than 18.5% of people with Crohn’s disease also have celiac disease. The study has “completely changed the way we can identify genetic risk factors,” says study co-author John D. Rioux, PhD, an associate professor of medicine at the University of Montreal, in Quebec, Canada. “There are sequence differences at the genetic level that get translated down to the protein levels,” Rioux notes. “And these differences may really nudge a person toward inflammation." He adds that "we’re just in the beginning, but we hope they may elucidate a common pathway and one day help us discover treatments that correct the underlying genetic changes.” Source: Jan. 27 issue of PLoS Genetics
Scott Adams posted an article in Dermatitis Herpetiformis: Skin Condition Associated with Celiac DiseaseThe following are links to sites have of dermatitis herpetiformis. Some of the photos are biopsies as seen through a microscope, and some are regular photographs of people with dermatitis herpetiformis, some of which are quite graphic. Pictures and an excellent article on dermatitis herpetiformis by Harold T. Pruessner, M.D., University of Texas Medical School at Houston: http://www.aafp.org/afp/980301ap/pruessn.html The University of Iowa: http://hardinmd.lib.uiowa.edu/dermnet/dermatitisherpetiformis.html Dermis.New Web Page: http://www.dermis.net/dermisroot/en/29366/diagnose.htm Medline: https://www.nlm.nih.gov/medlineplus/ency/article/001480.htm The Dermatitis Herpetiformis Online Community: http://www.dermatitisherpetiformis.org.uk/
Roy Jamron posted an article in The Origins of Celiac DiseaseCeliac.com 11/06/2008 - Previously, the possible link between gut bacteria and celiac disease has been discussed in "Do Vitamin D Deficiency, Gut Bacteria, and Gluten Combine in Infancy to Cause Celiac Disease?" A 5-year European study, DIABIMMUNE, is currently underway focusing on some 7000 children, from birth, investigating the development of intestinal bacterial flora and its influence on the development of the human immune system and autoimmune disease, including celiac disease. Hopefully, this study will provide some much needed answers. Now a Spanish group of scientists has produced further evidence supporting a possible role for gut bacteria in the pathogenesis of celiac disease by investigating whether gut microflora present in the feces of celiac disease patients participates in the pro-inflammatory activity of celiac disease. The makeup of fecal microflora in celiac disease patients differs significantly from that of healthy subjects. To determine whether gut microflora is a participant in the pro-inflammatory milieu of celiac disease, the Spanish research team incubated cultures of peripheral blood mononuclear cells from healthy adults with fecal microflora obtained from 26 active celiac disease children, 18 symptom-free celiac disease children on a gluten-free diet, and 20 healthy children. The scientists additionally investigated possible regulatory roles of Bifidobacterium longum ES1 and B. bifidum ES2 obtained from the feces of healthy individuals, co-incubating the Bifidobacterium with the test subject fecal microflora and the peripheral blood mononuclear cell culture. Fecal micrflora from both active and, notably, treated, symptom-free celiac children caused a significant increase in pro-inflammatory cytokine production and a decrease in anti-inflammatory IL-10 production in the peripheral blood mononuclear cell cultures compared to the fecal microflora from healthy children. However, cultures co-incubated with the Bifidobacterium strains exhibited a suppression of the pro-inflammatory cytokine production and an increase in IL-10 production. IL-10 is a cytokine which promotes immune tolerance. The scientists concluded that the makeup of the gut flora of celiacs may contribute to pro-inflammation in celiac disease, possibly in a synergy with gliadin, and that certain strains of Bifidobacterium appear to suppress and reverse pro-inflammatory effects and offering therapeutic opportunities for the treatment of celiac disease. It would have been interesting if the scientists had also investigated the effect of adding vitamin D to the fecal microflora and the peripheral blood mononuclear cell cultures. It is likely the addition of vitamin D might also have resulted in a suppression of pro-inflammatory cytokine production and an increase in IL-10 production. This is borne out by experiments with Mycobacterium tuberculosis and its culture filtrate antigen in peripheral blood mononuclear cell cultures where the addition of vitamin D resulted in a suppression of pro-inflammatory cytokine production and an increase in IL-10 production. It is possible that celiac disease may be entirely prevented in infancy by routinely administrating prophylactic doses of vitamin D and probiotics containing specific strains of Bifidobacterium before gluten is introduced into the infant's diet. The vitamin D and Bifidobacterium strains may provide an IL-10 anti-inflammatory environment in which the immune system learns to respond tolerantly to gluten, forever preventing the onset of celiac disease. The fact that certain strains of fecal Bifidobacterium from healthy individuals appear to suppress celiac disease inflammation brings to mind the concept of "fecal bacteriotherapy" or "fecal transplant", a therapy developed and used in practice by the world reknown Australian gastroenterologist, Prof. Thomas J. Borody, M.D., known best for his development of a triple-antibiotic treatment for H. pylori and ulcerative colitis. Fecal bacteriotherapy involves transplanting feces from a healthly, screened donor into an ailing patient with a persistant bacterial gastrointestinal disorder whose own gut flora has first been reduced or eliminated with antibiotics. The fecal microflora from the healthy donor reseeds the gut of the ailing patient with a healthy mix of intestinal microflora curing the gastrointestinal disorder. The Bifidobacterium research done by the Spanish researchers suggests that fecal bacteriotherapy might be an option to treat or cure celiac disease in adults, replacing gut flora causing intolerance to gluten with a healthy mix of gut flora that encourages tolerance to gluten. Sources  Do Vitamin D Deficiency, Gut Bacteria, and Gluten Combine in Infancy to Cause Celiac Disease? Roy S. Jamron https://www.celiac.com/articles/21605/  European Study Will Focus On Relation Of Gut Bacteria to Autoimmune Disease in Children Roy S. Jamron https://www.celiac.com/articles/21607/  Journal of Inflammation 2008, 5:19. Bifidobacterium strains suppress in vitro the pro-inflammatory milieu triggered by the large intestinal microbiota of coeliac patients. Medina M, De Palma G, Ribes-Koninckx C, Calabuig M, Sanza Y. http://www.journal-inflammation.com/content/pdf/1476-9255-5-19.pdf  J Clin Immunol. 2008 Jul;28(4):306-13. Regulatory role of promoter and 3' UTR variants of vitamin D receptor gene on cytokine response in pulmonary tuberculosis. Selvaraj P, Vidyarani M, Alagarasu K, Prabhu Anand S, Narayanan PR. http://www.springerlink.com/content/d67236620021j84u/  Prof. Thomas J. Borody, M.D., Bio and Publication List http://www.cdd.com.au/html/hospital/clinicalstaff/borody.html http://www.cdd.com.au/html/expertise/publications.html