Modifications of mesenteric adipose tissue during moderate experimental colitis in mice.
OBJECTIVE
Adipose tissue secretes various proteins referred to as adipokines, being involved in inflammation. It was recognized that mesenteric adipose tissue (MAT) is altered by inflammation, and pathologies such as inflammatory bowel disease (IBD). The aim of this study was to investigate the alterations of the mesenteric adipose tissue in two experimental colitis models in mice adapted to obtain moderate colonic inflammation.


METHODS
Colonic inflammation was obtained using two models, either DSS dissolved in drinking water or intra-colonic instillation of DNBS. The expression of adipokines (leptin and adiponectin) and inflammatory markers (IL-6, MCP-1, F4/80) was studied by qRT-PCR in the MAT of treated and control mice.


RESULTS
Observations of the colon and IL-6 plasma level determination demonstrated that DNBS treatment led to stronger inflammation. Colitis induced a decrease of mRNA encoding to leptin and adiponectin in MAT. In contrast, colonic inflammation led to an increase of mRNA encoding to IL-6, MCP-1 and F4/80, a specific marker of macrophages.


CONCLUSIONS
The mesenteric adipose tissue, in two models of moderate colitis, shows a loss of adipose profile and a strong increase of inflammatory pattern, close to the observations made in MAT of IBD patients. These data suggest that these pro-inflammatory modifications of MAT have to be taken into account in the pathophysiology of IBD.
INRA, UMR 1331 Toxalim, Neuro-Gastroenterology & Nutrition Group, Toulouse, France; University of Toulouse, EI-Purpan, UMR 1331 Toxalim, Neuro-Gastroenterology & Nutrition Group, Toulouse, France.
Isabelle
I
Olivier
INRA, UMR 1331 Toxalim, Neuro-Gastroenterology & Nutrition Group, Toulouse, France; University of Toulouse, EI-Purpan, UMR 1331 Toxalim, Neuro-Gastroenterology & Nutrition Group, Toulouse, France. Electronic address: vtheodor@toulouse.inra.fr.
Vassilia
V
Theodorou
INSERM, I2MR, Adipocyte Secretions, Obesities and Associated Pathologies Team, Toulouse, France.
Philippe
P
Valet
INSERM, I2MR, Adipocyte Secretions, Obesities and Associated Pathologies Team, Toulouse, France.
Isabelle
I
Castan-Laurell
INRA, UMR 1331 Toxalim, Neuro-Gastroenterology & Nutrition Group, Toulouse, France; University of Toulouse, EI-Purpan, UMR 1331 Toxalim, Neuro-Gastroenterology & Nutrition Group, Toulouse, France.
Laurent
L
Ferrier
INRA, UMR 1331 Toxalim, Neuro-Gastroenterology & Nutrition Group, Toulouse, France; University of Toulouse, EI-Purpan, UMR 1331 Toxalim, Neuro-Gastroenterology & Nutrition Group, Toulouse, France.
Hélène
H
Eutamène
D052242:Adiponectin / Q000378:metabolism*; D000273:Adipose Tissue / Q000378:metabolism*; D000818:Animals; D003092:Colitis / Q000503:physiopathology*; D016264:Dextran Sulfate / Q000633:toxicity; D004139:Dinitrofluorobenzene / Q000031:analogs & derivatives / Q000633:toxicity; D004195:Disease Models, Animal; D007249:Inflammation / Q000503:physiopathology*; D018836:Inflammation Mediators / Q000378:metabolism; D015212:Inflammatory Bowel Diseases / Q000503:physiopathology; D020738:Leptin / Q000378:metabolism*; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D046988:Proteasome Endopeptidase Complex / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction
D052242:Adiponectin; D018836:Inflammation Mediators; D020738:Leptin; D012333:RNA, Messenger; C045305:2,4-dinitrofluorobenzene sulfonic acid; D016264:Dextran Sulfate; D004139:Dinitrofluorobenzene; D046988:Proteasome Endopeptidase Complex
Adipose tissue; Experimental colitis; Inflammatory bowel disease