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This review discusses the role of the pancreatic-gut axis in controlling pathobionts and intestinal inflammation.
[ABSTRACT]The imbalance of bacterial communities, known as “dysbiosis”, is thought to be not only correlated with but also the cause of diseases. Recently, it has been considered that the colonization of intestinal bacteria into normally sterile host tissues or extra-intestinal compartments, known as bacterial translocation, causes tissue damage and induces the development of inflammatory diseases. Inflammatory bowel disease (IBD) is linked to bacterial translocation that exacerbate intestinal inflammation by promoting excessive host immune responses or impairing the mucosal barrier. These potentially translocated bacteria are known as pathobionts, defined as symbionts that can promote pathology only when specific genetic, immunological, or environmental conditions are altered in the host. In this review, I herein discuss the current understanding of the host mucosal defense, specifically with regard to the pancreas–intestinal barrier axis, for the control of pathobionts in intestinal inflammation.
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Yosuke Kurashima (2023) studied this question.
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