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2015 ; 43
(4
): 727-33
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The intestinal immunoendocrine axis: novel cross-talk between enteroendocrine
cells and the immune system during infection and inflammatory disease
#MMPMID26551720
Worthington JJ
Biochem Soc Trans
2015[Aug]; 43
(4
): 727-33
PMID26551720
show ga
The intestinal epithelium represents one of our most important interfaces with
the external environment. It must remain tightly balanced to allow nutrient
absorption, but maintain barrier function and immune homoeostasis, a failure of
which results in chronic infection or debilitating inflammatory bowel disease
(IBD). The intestinal epithelium mainly consists of absorptive enterocytes and
secretory goblet and Paneth cells and has recently come to light as being an
essential modulator of immunity as opposed to a simple passive barrier. Each
epithelial sub-type can produce specific immune modulating factors, driving
innate immunity to pathogens as well as preventing autoimmunity. The
enteroendocrine cells comprise just 1% of this epithelium, but collectively form
the bodies' largest endocrine system. The mechanisms of enteroendocrine cell
peptide secretion during feeding, metabolism and nutrient absorption are well
studied; but their potential interactions with the enriched numbers of
surrounding immune cells remain largely unexplored. This review focuses on
alterations in enteroendocrine cell number and peptide secretion during
inflammation and disease, highlighting the few in depth studies which have
attempted to dissect the immune driven mechanisms that drive these phenomena.
Moreover, the emerging potential of enteroendocrine cells acting as innate
sensors of intestinal perturbation and secreting peptides to directly orchestrate
immune cell function will be proposed. In summary, the data generated from these
studies have begun to unravel a complex cross-talk between immune and
enteroendocrine cells, highlighting the emerging immunoendocrine axis as a
potential target for therapeutic strategies for infections and inflammatory
disorders of the intestine.