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DNBS/TNBS Colitis Models: Providing Insights Into Inflammatory Bowel Disease and Effects of Dietary Fat
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Mesenteric fat - control site for bacterial translocation in colitis?
A Batra1, M M Heimesaat, S Bereswill
1Medical department I, Charité-Universitätsmedizin Berlin, Campus Benjamin Franklin, Berlin, Germany.
Mucosal Immunology
|May 10, 2012
Summary
In Crohn's disease, mesenteric fat responds to bacterial translocation during inflammation by releasing cytokines and recruiting immune cells. This adipose tissue plays a protective role against bacterial invasion.
Area of Science:
- Immunology
- Gastroenterology
- Adipose Tissue Biology
Background:
- Crohn's disease involves bacterial presence in mesenteric fat, a tissue with unknown inflammatory functions.
- Bacterial translocation into mesenteric fat is observed during intestinal inflammation.
Purpose of the Study:
- To define the effector responses of mesenteric fat to bacterial translocation during intestinal inflammation.
- To investigate the innate immune functions of mesenteric fat and epithelium.
Main Methods:
- Dextran sulfate sodium-induced colitis model in mice.
- Evaluation of peptide and bacterial translocation into mesenteric fat.
- Characterization of mesenteric fat and epithelial functions at tissue, cellular, and molecular levels.
- Studies in wild-type (WT) and MyD88(-/-) mice.
- In vitro studies with preadipocytes and bacterial products.
Main Results:
- Oral peptides translocated in healthy WT mice; bacterial translocation increased in chronic colitis.
- Mesenteric fat from colitic mice showed elevated cytokine release and immune cell infiltration.
- MyD88(-/-) mice exhibited bacterial translocation in health and increased translocation in colitis.
- Cytokine production in mesenteric fat was less pronounced in MyD88(-/-) mice compared to WT mice during colitis.
- In vitro, fat and preadipocytes increased cytokine production upon exposure to bacterial products and demonstrated phagocytic activity.
Conclusions:
- Mesenteric fat exhibits significant cytokine production and immune cell infiltration during colonic inflammation.
- These responses in mesenteric fat are considered protective mechanisms against bacterial translocation.
- MyD88 signaling pathway influences the mesenteric fat response to bacterial translocation.
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