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Jefferson Adams posted an article in Celiac Disease & Gluten Intolerance ResearchCeliac.com 07/28/2016 - Celiac disease is an immune-mediated enteropathy triggered by gluten in genetically susceptible individuals. Researchers know that innate immunity plays a role in triggering celiac disease, but they don't understand the connection very well at all. Although previous in vitro work suggests that gliadin peptide p31-43 acts as an innate immune trigger, the underlying pathways are unclear and have not been explored in vivo. The research team included RE Araya, MF Gomez Castro, P Carasi, JL McCarville, J Jury, AM Mowat, EF Verdu, and FG Chirdo. They are variously affiliated with the Instituto de Estudios Inmunológicos y Fisiopatológicos (IIFP)(CONICET-UNLP), Facultad de Ciencias Exactas, Universidad Nacional de La Plata, La Plata, Argentina; the Catedra de Microbiología, Facultad de Ciencias Exactas, Universidad Nacional de La Plata, La Plata, Argentina; the Farncombe Family Digestive Health Research Institute, McMaster University, Hamilton, Ontario, Canada; the Centre for Immunobiology, Institute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow, Scotland, United Kingdom; and with the Instituto de Estudios Inmunológicos y Fisiopatológicos (IIFP)(CONICET-UNLP), Facultad de Ciencias Exactas, Universidad Nacional de La Plata, La Plata, Argentina. Their team observed that introduction of p31-43 into the gut of normal mice causes structural changes in the small intestinal mucosa consistent with those seen in celiac disease, including increased cell death and expression of inflammatory mediators. The effects of p31-43 were dependent on MyD88 and type I IFNs, but not Toll-like receptor 4 (TLR4), and were enhanced by co-administration of the TLR3 agonist polyinosinic:polycytidylic acid. Together, these results indicate that gliadin peptide p31-43 activates celiac-related innate immune pathways in vivo, such as IFN-dependent inflammation. These findings also suggest a common mechanism for the potential interaction between dietary gluten and viral infections in the pathogenesis of celiac disease, meaning that certain viral infections may pave the way for celiac disease to develop. Source: Am J Physiol Gastrointest Liver Physiol. 2016 Jul 1;311(1):G40-9. doi: 10.1152/ajpgi.00435.2015. Epub 2016 May 5.
Jefferson Adams posted an article in Celiac Disease & Gluten Intolerance ResearchCeliac.com 05/12/2016 - What is the impact of locally formulated gluten-free flour on the dietary pattern of Pakistani celiac patients? A research team recently set out to introduce indigenously formulated gluten free flour (GFF) in the diets of selected Pakestani celiac patients, and to investigate the impact of formulated gluten-free flour on the dietary pattern of those patients. The researchers included Samia Kalsoom and Saeed Ahmad Nagra of the Government College of Home Economics in Lahore, Pakistan, and the Institue of Chemistry, University of the Punjab in Lahore, Pakistan. The flour used in the study was formulated using indigenous sources of rice, corn and daal mung. The researchers then selected fifty diagnosed celiac patients from Sheikh Zayed Medical Complex, and the Mayo Hospital in Lahore, Pakistan, and provided those patients with gluten-free flour for a period of four months. The researchers conducted pre- and post treatment assessments of food intake, compliance, appetite, meal patterns and meal satisfaction of the study participants. Both before and during the feeding trial, the study participants received caloric and macronutrient levels above the recommended dietary guidelines. Mean carbohydrate exchanges of all age groups were higher than standard recommended values for their respective age groups. Before the feeding trial, participants of 19 to 30 years of age reported the highest gluten consumption. These levels fell significantly with GFF induction. Meanwhile milk, meat, fruit and vegetable intake of the study participants was less than the recommended intake levels. Study participants of 9-13 years had the highest flour consumption, but there was no significant difference was found in the food intake from starch, milk, meat and fruit groups during the treatment phase. A significant increase in vegetable intake was observed with GFF administration. All age groups showed improved compliance, appetite, meal regularity and meal satisfaction, with children showing the most pronounced changes. Source: Pakistan J. Zool., vol. 48(2), pp. 415-422, 2016.
Jefferson Adams posted an article in Celiac Disease & Gluten Intolerance ResearchCeliac.com 07/21/2014 - The presence of HLA haplotype DR3–DQ2 or DR4–DQ8 is associated with an increased risk of celiac disease. In addition, nearly all children with celiac disease have serum antibodies against tissue transglutaminase (tTG). A research team recently set out to determine the risk of celiac disease autoimmunity and celiac disease, by age and by halpotype, in children. The research team included Edwin Liu, M.D., Hye-Seung Lee, Ph.D., Carin A. Aronsson, M.Sc., William A. Hagopian, M.D., Ph.D., Sibylle Koletzko, M.D., Ph.D., Marian J. Rewers, M.D., M.P.H., George S. Eisenbarth, M.D., Ph.D., Polly J. Bingley, M.D., Ezio Bonifacio, Ph.D., Ville Simell, M.Sc., and Daniel Agardh, M.D., Ph.D. for the TEDDY Study Group. The team studied 6403 children with HLA haplotype DR3–DQ2 or DR4–DQ8 prospectively from birth in the United States, Finland, Germany, and Sweden. The study’s primary end point was the development of celiac disease autoimmunity, which the team defined as the presence of tTG antibodies on two consecutive tests at least 3 months apart. The secondary end point was the development of celiac disease itself, which they defined as either a diagnosis on biopsy or persistently high levels of tTG antibodies. The average follow-up was 5 years, with an overall range of 46 to 77 months. A total of 786 children (12%) developed celiac disease autoimmunity. A total of 350 children underwent biopsy, and 291 of those were diagnosed with celiac disease. Another 21 children did not undergo biopsy, but showed persistently high levels of tTG antibodies. For children with a single DR3–DQ2 haplotype, rates of celiac disease autoimmunity and celiac disease by the age of 5 years were 11% and 3%, respectively. For those with two copies (DR3–DQ2 homozygosity) rates of celiac disease autoimmunity and celiac disease by the age of 5 years were 26% and 11%, respectively. The adjusted hazard ratios for celiac disease autoimmunity were 2.09 (95% confidence interval [CI], 1.70 to 2.56) among children with one gene, and 5.70 (95% CI, 4.66 to 6.97) among children with both genes, as compared with children who had the lowest-risk genotypes (DR4–DQ8 heterozygotes or homozygotes). Living in Sweden was also independently associated with an increased risk of celiac disease autoimmunity (hazard ratio, 1.90; 95% CI, 1.61 to 2.25). Children with the HLA haplotype DR3–DQ2, especially homozygotes, were found to be at high risk for celiac disease autoimmunity and celiac disease early in childhood. People in Sweden face a higher risk for celiac disease autoimmunity and celiac disease than residents of other countries. These finding highlight the importance of studying environmental factors associated with celiac disease. Source: N Engl J Med 2014; 371:42-49July 3, 2014. DOI: 10.1056/NEJMoa1313977