title: Role of fat and adipokines in intestinal inflammation.
abstract: OBJECTIVE
  This review summarizes current knowledge on the contribution of mesenteric adipose tissue in intestinal inflammation. We will describe the cellular and humoral characteristics of creeping fat, their potential impact for Crohn's disease and propose a working model for the critical interplay between the creeping fat and the inflamed intestine.
  
  
  RESULTS
  Creeping fat can be distinguished from healthy adipose tissue by its distinctively small adipocytes, by a specific microenvironment defined by high levels of adipokines and by a dominant immune cell infiltration. In Crohn's disease transmural inflammation facilitates increased bacterial translocation into the creeping fat. Translocalizing antigens can directly activate (pre)adipocytes via innate receptors. Adipocyte-derived mediators modulate phenotype and function of innate and adaptive immune cells. Activated (pre)adipocytes and adipokine-modulated immune cells might support a degree of inflammatory activation within the creeping fat that allows competent immune defense against exogenous factors while preventing systemic inflammation.
  
  
  CONCLUSIONS
  Fat tissue as an active organ in health and disease has been ignored for too long. The last few years of research provided evidence for the complex metabolic and immunological functions of adipose tissue. On the basis of the available data, creeping fat in Crohn's disease exerts a protective function by a localized anti-inflammatory effect, thus preventing a systemic inflammatory response.
authors.affiliation: Medical Department (Gastroenterology, Rheumatology, Infectious Diseases), Charité - Universitätsmedizin Berlin, Campus Benjamin Franklin, Berlin, Germany.
authors.forename: LeaI
authors.initials: L
authors.lastname: Kredel
authors.forename: Arvind
authors.initials: A
authors.lastname: Batra
authors.forename: Britta
authors.initials: B
authors.lastname: Siegmund
mesh_terms: D054392:Adipokines / Q000378:metabolism*; D000273:Adipose Tissue / Q000378:metabolism*; D015415:Biomarkers / Q000378:metabolism; D006801:Humans; D007249:Inflammation / Q000276:immunology* / Q000378:metabolism; D018836:Inflammation Mediators / Q000378:metabolism*; D015212:Inflammatory Bowel Diseases / Q000276:immunology* / Q000378:metabolism; D007413:Intestinal Mucosa / Q000276:immunology* / Q000378:metabolism; D020738:Leptin / Q000378:metabolism; D050356:Lipid Metabolism / Q000276:immunology*; D008643:Mesentery / Q000276:immunology* / Q000378:metabolism; D054419:Receptors, Adiponectin / Q000378:metabolism; D011956:Receptors, Cell Surface / Q000378:metabolism; D054411:Receptors, Leptin / Q000378:metabolism; D052243:Resistin / Q000378:metabolism
chemical_list: D054392:Adipokines; D015415:Biomarkers; D018836:Inflammation Mediators; D020738:Leptin; D054419:Receptors, Adiponectin; D011956:Receptors, Cell Surface; D054411:Receptors, Leptin; D052243:Resistin