Abstract

Immune Activation in Functional Gastrointestinal Disorders

Burns G1,2,3,4,5, Pryor J1,2,3,4,5, Holtmann G1,2,3,4,5, Walker MM1,2,3,4,5, Talley NJ1,2,3,4,5, Keely S1,2,3,4,5. Gastroenterol Hepatol (N Y). 2019 Oct;15(10):539-548.

 
     

Author information

Ms Burns is a PhD graduate student, Ms Pryor is an undergraduate research student.

Dr Walker is a professor of anatomical pathology.

Dr Talley is a laureate professor.

Dr Keely is an associate professor in the Priority Research Centre for Digestive Health and Neurogastroenterology in the Faculty of Health and Medicine at the University of Newcastle in Callaghan, New South Wales, Australia, as well as in the Hunter Medical Research Institute in New Lambton Heights, New South Wales, Australia.

Dr Holtmann is director of gastroenterology and hepatology at the Princess Alexandra Hospital in Brisbane, Queensland, Australia and a professor in the Faculty of Medicine at the University of Queensland in Woolloongabba, Queensland, Australia.

Abstract

There is growing appreciation that functional gastrointestinal disorders (FGIDs) such as functional dyspepsia and irritable bowel syndrome are heterogeneous conditions linked by subtle inflammation within the gastrointestinal (GI) tract. The literature suggests that while the symptoms of these diseases may manifest with similar clinical presentations, there are significant differences in triggers and disease severity among patients classified into the same subtype. It is hypothesized that the subtle inflammation observed in these patients is related to an imbalance in GI homeostasis. Disruption of the delicate homeostatic balance within the GI tract can result from any number or combination of factors, including dysbiosis, loss of barrier integrity, genetic predisposition, or immune responses to dietary or luminal antigens. This article discusses the interplay between the immune system, microbiota, and luminal environment in FGIDs. In addition, the article proposes emerging immune pathways, including those involving T-helper type 17 response and innate lymphoid cells, as potential regulators of the subtle inflammation characteristic of FGIDs that warrant investigation in future studies.

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