Role of adipose tissue and HO-1 in modulation of inflammatory response: a study in an experimental model of colitis.

• Grant number: 11/21541-4
• Support type: Scholarships in Brazil - Scientific Initiation
• Effective date (Start): February 01, 2012
• Effective date (End): January 31, 2014
• Field of knowledge: Health Sciences - Medicine - Medical Clinics
• Principal researcher: Niels Olsen Saraiva Câmara
• Grantee: Denis Gonçalves Silva
• Home Institution: Escola Paulista de Medicina (EPM). Universidade Federal de São Paulo (UNIFESP). Campus São Paulo. São Paulo , SP, Brazil

Abstract

In recent decades, the transformation of lifestyle, and in particular the changes in dietary patterns determined an widespread epidemic unprecedented in human history, obesity. The adipose tissue contributes to the production of proinflammatory molecules (cytokines, chemotactic factors and adipokines) involved in the state of low-grade chronic systemic inflammation observed in obesity.An important factor related to the control of food intake and obesity that can modulate the immune system is leptin. Several studies have implicated leptin in the pathogenesis of autoimmune inflammatory conditions such as colitis. The mesenteric adipose tissue hypertrophy and changes in the production of adipokines are features present in patients with colitis. Experimentally, these changes can be obtained in animals with colitis induced by dextran sulfate sodium (DSS). But it is not clear whether leptin has a pro-inflammatory or anti-inflammatory role in the pathogenesis of inflammatory bowel condition.Thus, due to the actions of leptin in favor of proliferation of regulatory T cells, and leptin and the cytokines IL-12 and IFN-g in polarizing the Th1 cells, it is likely that in obese mice induced by high calorie diet the state of low-grade chronic systemic inflammation increases the severity of inflammatory diseases such as colitis. So we have the objective to study the possible role of obesity in a model of ulcerative colitis as well as possible mechanisms of this disease.