- Safe Gluten-Free Food List (Safe Ingredients)
- Unsafe Gluten-Free Food List (Unsafe Ingredients)
- Gluten-Free Alcoholic Beverages
- Celiac Disease Symptoms
- The Gluten-Free Diet 101 - A Beginner's Guide to Going Gluten-Free
- Interpretation of Celiac Disease Blood Test Results
- Is Buckwheat Flour Really Gluten-Free?
Study Hints at Connection Between Celiac Disease and Certain Viral Infections
Jefferson Adams is a freelance writer living in San Francisco. His poems, essays and photographs have appeared in Antioch Review, Blue Mesa Review, CALIBAN, Hayden's Ferry Review, Huffington Post, the Mississippi Review, and Slate among others.
He is a member of both the National Writers Union, the International Federation of Journalists, and covers San Francisco Health News for Examiner.com.View all articles by Jefferson Adams
Photo: CC--Todd Chandler
Celiac.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.
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.
- Am J Physiol Gastrointest Liver Physiol. 2016 Jul 1;311(1):G40-9. doi: 10.1152/ajpgi.00435.2015. Epub 2016 May 5.
Celiac.com welcomes your comments below (registration is NOT required).