title: The combination of high-fat diet-induced obesity and chronic ulcerative colitis reciprocally exacerbates adipose tissue and colon inflammation.
abstract: BACKGROUND
  This study evaluated the relationship between ulcerative colitis and obesity, which are both chronic diseases characterized by inflammation and increases in immune cells and pro-inflammatory cytokines.
  
  
  METHODS
  Mice with chronic ulcerative colitis induced by 2 cycles of dextran sodium sulfate (DSS) in the first and fourth week of the experiment were fed a high-fat diet (HFD) to induce obesity by 8 weeks. The animals were divided into 4 \ groups (control, colitis, HFD and colitis + HFD).
  
  
  RESULTS
  Obesity alone did not raise histopathology scores, but the combination of obesity and colitis worsened the scores in the colon compared to colitis group. Despite the reduction in weight gain, there was increased inflammatory infiltrate in both the colon and visceral adipose tissue of colitis + HFD mice due to increased infiltration of macrophages, neutrophils and lymphocytes. Intravital microscopy of VAT microvasculature showed an increase in leukocyte adhesion and rolling and overexpression of adhesion molecules compared to other groups. Moreover, circulating lymphocytes, monocytes and neutrophils in the spleen and cecal lymph nodes were increased in the colitis + HFD group.
  
  
  CONCLUSIONS
  Our results demonstrated the relationship between ulcerative colitis and obesity as aggravating factors for each disease, with increased inflammation in the colon and adipose tissue and systemic alterations observed in the spleen, lymph nodes and bloodstream.
authors.affiliation: Department of Biochemistry and Immunology - Institute of Biological Sciences -Universidade Federal de Minas Gerais, Av, Antonio Carlos, 6627, Pampulha, Belo Horizonte, MG CEP: 31270-901, Brazil. lilianteixeiranutricao@gmail.com
authors.forename: Lílian G
authors.initials: LG
authors.lastname: Teixeira
authors.forename: Alda J
authors.initials: AJ
authors.lastname: Leonel
authors.forename: Edenil C
authors.initials: EC
authors.lastname: Aguilar
authors.forename: Nathália V
authors.initials: NV
authors.lastname: Batista
authors.forename: Andréa C
authors.initials: AC
authors.lastname: Alves
authors.forename: Candido C
authors.initials: CC
authors.lastname: Coimbra
authors.forename: Adaliene V M
authors.initials: AV
authors.lastname: Ferreira
authors.forename: Ana Maria C
authors.initials: AM
authors.lastname: de Faria
authors.forename: Denise C
authors.initials: DC
authors.lastname: Cara
authors.forename: Jacqueline I
authors.initials: JI
authors.lastname: Alvarez Leite
mesh_terms: D054392:Adipokines / Q000097:blood; D000273:Adipose Tissue / Q000098:blood supply / Q000473:pathology*; D050154:Adiposity; D000818:Animals; D015703:Antigens, CD / Q000378:metabolism; D018925:Chemokines / Q000378:metabolism; D003093:Colitis, Ulcerative / Q000139:chemically induced* / Q000150:complications* / Q000473:pathology; D003106:Colon / Q000473:pathology; D016207:Cytokines / Q000378:metabolism; D016264:Dextran Sulfate; D059305:Diet, High-Fat; D004822:Epididymis / Q000473:pathology; D015870:Gene Expression; D007249:Inflammation; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D055806:Microvessels / Q000473:pathology; D009765:Obesity / Q000150:complications* / Q000473:pathology; D054411:Receptors, Leptin / Q000235:genetics / Q000378:metabolism; D013601:T-Lymphocytes / Q000378:metabolism / Q000473:pathology; D051197:Toll-Like Receptor 4 / Q000235:genetics / Q000378:metabolism
chemical_list: D054392:Adipokines; D015703:Antigens, CD; D018925:Chemokines; D016207:Cytokines; D054411:Receptors, Leptin; D051197:Toll-Like Receptor 4; D016264:Dextran Sulfate
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