title: Inflammatory cytokine gene expression in mesenteric adipose tissue during acute experimental colitis.
abstract: BACKGROUND
  Production of inflammatory cytokines by mesenteric adipose tissue (MAT) has been implicated in the pathogenesis of inflammatory bowel disease (IBD). Animal models of colitis have demonstrated inflammatory changes within MAT, but it is unclear if these changes occur in isolation or as part of a systemic adipose tissue response. It is also unknown what cell types are responsible for cytokine production within MAT. The present study was designed to determine whether cytokine production by MAT during experimental colitis is depot-specific, and also to identify the source of cytokine production within MAT.
  
  
  METHODS
  Experimental colitis was induced in 6-month-old C57BL/6 mice by administration of dextran sulfate sodium (2% in drinking water) for up to 5 days. The induction of cytokine mRNA within various adipose tissues, including mesenteric, epididymal, and subcutaneous, was analyzed by qRT-PCR. These adipose tissues were also examined for histological evidence of inflammation. The level of cytokine mRNA during acute colitis was compared between mature mesenteric adipocytes, mesenteric stromal vascular fraction (SVF), and mesenteric lymph nodes.
  
  
  RESULTS
  During acute colitis, MAT exhibited an increased presence of infiltrating mononuclear cells and fibrotic structures, as well as decreased adipocyte size. The mRNA levels of TNF-α, IL-1β, and IL-6 were significantly increased in MAT but not other adipose tissue depots. Within the MAT, induction of these cytokines was observed mainly in the SVF.
  
  
  CONCLUSIONS
  Acute experimental colitis causes a strong site-specific inflammatory response within MAT, which is mediated by cells of the SVF, rather than mature adipocytes or mesenteric lymph nodes.
authors.affiliation: Markey Cancer Center, University of Kentucky, Lexington, Kentucky, United States of America ; Department of Surgery, University of Kentucky, Lexington, Kentucky, United States of America.
authors.forename: W Conan
authors.initials: WC
authors.lastname: Mustain
authors.affiliation: Markey Cancer Center, University of Kentucky, Lexington, Kentucky, United States of America ; Department of Surgery, University of Kentucky, Lexington, Kentucky, United States of America.
authors.forename: Marlene E
authors.initials: ME
authors.lastname: Starr
authors.affiliation: Markey Cancer Center, University of Kentucky, Lexington, Kentucky, United States of America ; Department of Surgery, University of Kentucky, Lexington, Kentucky, United States of America.
authors.forename: Joseph D
authors.initials: JD
authors.lastname: Valentino
authors.affiliation: Department of Microbiology, Immunology, and Molecular Genetics, University of Kentucky, Lexington, Kentucky, United States of America.
authors.forename: Donald A
authors.initials: DA
authors.lastname: Cohen
authors.affiliation: Markey Cancer Center, University of Kentucky, Lexington, Kentucky, United States of America ; Department of Surgery, University of Kentucky, Lexington, Kentucky, United States of America.
authors.forename: Daiki
authors.initials: D
authors.lastname: Okamura
authors.affiliation: Markey Cancer Center, University of Kentucky, Lexington, Kentucky, United States of America ; Department of Biostatistics, University of Kentucky, Lexington, Kentucky, United States of America.
authors.forename: Chi
authors.initials: C
authors.lastname: Wang
authors.affiliation: Markey Cancer Center, University of Kentucky, Lexington, Kentucky, United States of America ; Department of Surgery, University of Kentucky, Lexington, Kentucky, United States of America.
authors.forename: B Mark
authors.initials: BM
authors.lastname: Evers
authors.affiliation: Markey Cancer Center, University of Kentucky, Lexington, Kentucky, United States of America ; Department of Surgery, University of Kentucky, Lexington, Kentucky, United States of America ; Department of Physiology, University of Kentucky, Lexington, Kentucky, United States of America.
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Saito
mesh_terms: D000208:Acute Disease; D000273:Adipose Tissue / Q000378:metabolism* / Q000473:pathology*; D000818:Animals; D003092:Colitis / Q000139:chemically induced / Q000235:genetics* / Q000378:metabolism / Q000473:pathology*; D016207:Cytokines / Q000097:blood / Q000235:genetics* / Q000378:metabolism; D016264:Dextran Sulfate / Q000009:adverse effects; D004195:Disease Models, Animal; D018450:Disease Progression; D015870:Gene Expression; D007249:Inflammation / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D018836:Inflammation Mediators / Q000378:metabolism; D008297:Male; D008643:Mesentery / Q000378:metabolism / Q000473:pathology; D051379:Mice; D013997:Time Factors
chemical_list: D016207:Cytokines; D018836:Inflammation Mediators; D016264:Dextran Sulfate