Perspectives on Adipose Tissue, Chagas Disease and Implications for the Metabolic Syndrome

[摘要] The contribution of adipose tissue an autocrine and endocrine organ in the pathogenesis of infectious disease and metabolic syndrome is gaining attention. Adipose tissue and adipocytes are one of the major targets ofT. cruziinfection. Parasites are detected 300 days postinfection in adipose tissue. Infection of adipose tissue and cultured adipocytes triggered localexpression of inflammatory mediators resulting in the upregulation of cytokine and chemokinelevels. Adipose tissue obtained from infected mice display an increased infiltration ofinflammatory cells. Adiponectin, an adipocyte specific protein, which exerts antiinflammatoryeffects, is reduced during the acute phase of infection. The antiinflammatory regulatorperoxisome proliferator activated receptor-γ(PPAR-γ) is downregulated in infected culturedadipocytes and adipose tissue.T. cruziinfection is associated with an upregulation of signalingpathways such as MAPKs, Notch and cyclin D, and reduced caveolin-1 expression. Adiponectin null mice have a cardiomyopathy and thus we speculate that theT. cruzi-inducedreduction in adiponectin contributes to theT. cruzi-induced cardiomyopathy. WhileT. cruziinfection causes hypoglycemia which correlates with mortality, hyperglycemia is associatedwith increased parasitemia and mortality. TheT. cruzi-induced increase in macrophages inadipose tissue taken together with the reduction in adiponectin and the associatedcardiomyopathy is reminiscent of the metabolic syndrome.

[学科分类] 传染病学