Mesenteric fat - control site for bacterial translocation in colitis?

Mucosal Immunology
A BatraB Siegmund

Abstract

In Crohn's disease bacteria could be detected in the adjacent mesenteric fat characterized by hypertrophy of unknown function. This study aimed to define effector responses of this compartment induced by bacterial translocation during intestinal inflammation. Dextran sulfate sodium-induced colitis served as a model of intestinal inflammation. Translocation of peptides and bacteria into mesenteric fat was evaluated. Innate functions of mesenteric fat and epithelium were characterized at whole tissue, cellular, and effector molecule levels. Orally applied peptides translocated in healthy wild-type (WT) mice. Bacterial translocation was not detected in healthy and acute but increased in chronic colitis. Mesenteric fat from colitic mice released elevated levels of cytokines and was infiltrated by immune cells. In MyD88(-/-) mice bacterial translocation occurred in health and increased in colitis. The exaggerated cytokine production in mesenteric fat accompanying colonic inflammation in WT mice was less distinct in MyD88(-/-) mice. In vitro studies revealed that fat not only increases cytokine production following contact with bacterial products, but also that preadipocytes are potent phagocytes. Colonic inflammation is accompanied ...Continue Reading

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Apr 16, 2014·Journal of Crohn's & Colitis·Giovanni LatellaIan C Lawrance
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May 1, 2021·International Journal of Molecular Sciences·Eva KaraskovaDavid Karasek
Sep 17, 2021·Journal of Crohn's & Colitis·Roger SuauJosep Manyé

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