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The Complex Relationship Between Microbiota, Immune Response and Creeping Fat in Crohn's Disease

期刊

JOURNAL OF CROHNS & COLITIS
卷 16, 期 3, 页码 472-489

出版社

OXFORD UNIV PRESS
DOI: 10.1093/ecco-jcc/jjab159

关键词

Creeping fat; Crohn's disease; microbiota

资金

  1. Instituto Carlos III-General Evaluation Branch
  2. European Regional Development Fund [PI09/1294, PI12/00621, PI18/00892, PI20/00420]
  3. Centro de Investigacion Biomedica en Red (CIBER, Gobierno de Espana) [CB06_04_0034]
  4. AGAUR, Generalitat de Catalunya [2017 SGR 1217]

向作者/读者索取更多资源

In recent years, there has been a growing interest in the pathological involvement of creeping fat in Crohn's disease (CD). Despite its protective nature, the abnormal inflammatory activity of creeping fat may worsen the severity of CD, and the inflammatory process associated with CD involves various cellular and molecular changes.
In the last decade, there has been growing interest in the pathological involvement of hypertrophic mesenteric fat attached to the serosa of the inflamed intestinal segments involved in Crohn's disease [CD], known as creeping fat. In spite of its protective nature, creeping fat harbours an aberrant inflammatory activity which, in an already inflamed intestine, may explain why creeping fat is associated with a greater severity of CD. The transmural inflammation of CD facilitates the interaction of mesenteric fat with translocated intestinal microorganisms, contributing to activation of the immune response. This may be not the only way in which microorganisms alter the homeostasis of this fatty tissue: intestinal dysbiosis may also impair xenobiotic metabolism. All these CD-related alterations have a functional impact on nuclear receptors such as the farnesoid X receptor or the peroxisome proliferator-activated receptor gamma, which are implicated in regulation of the immune response, adipogenesis and the maintenance of barrier function, as well as on creeping fat production of inflammatory-associated cells such as adipokines. The dysfunction of creeping fat worsens the inflammatory course of CD and may favour intestinal fibrosis and fistulizing complications. However, our current knowledge of the pathophysiology and pathogenic role of creeping fat is controversial and a better understanding might provide new therapeutic targets for CD. Here we aim to review and update the key cellular and molecular alterations involved in this inflammatory process that link the pathological components of CD with the development of creeping fat.

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