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.

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.

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