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Cytokines and Intestinal Mucosal Immunity

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Front. Immunol. | doi: 10.3389/fimmu.2018.01974

Adipokines and their role in intestinal inflammation

  • 1Medicine (Gastroenterology, Infectious Diseases, Rheumatology), Charité Universitätsmedizin Berlin, Germany

Fat tissue was initially described for its endocrine and metabolic function. Over the last two decades increasing evidence indicated a close interaction with the immune system. Partly responsible for this immunodulatory function is soluble factors released by the fat tissue, most prominently the so-called adipokines. These discoveries led to the question how adipokines influence inflammatory diseases. Linking inflammation and adipose tissue, Crohn's disease, a chronic inflammatory bowel disease, is of particular interest for studying the immune modulatory properties of adipokines since it is characterized by a hyperplasia of the mesenteric fat that subsequently is creeping around the inflamed segments of the small intestine. Thus, the role of several adipokines in the creeping fat as well as in intestinal inflammation was recently explored. The present review selected the four adipokines adiponectin, apelin, chemerin and leptin and provides a working model based on the available literature how these factors participate in the maintenance of intestinal immune homeostasis.

Keywords: Adipokines, inflammatory bowel disease, Crohn's disease, Creeping fat, Cytokines

Received: 27 May 2018; Accepted: 10 Aug 2018.

Edited by:

Fabio Cominelli, Case Western Reserve University, United States

Reviewed by:

Angela Bonura, Consiglio Nazionale Delle Ricerche (CNR), Italy
Giovanna Montana, Istituto di biomedicina e di immunologia molecolare Alberto Monroy (IBIM), Italy  

Copyright: © 2018 Weidinger, Ziegler, Letizia, Schmidt and Siegmund. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: Prof. Britta Siegmund, Charité Universitätsmedizin Berlin, Medicine (Gastroenterology, Infectious Diseases, Rheumatology), Berlin, Germany,