[Role of cytokines in resistance and pathology in Trypanosoma cruzi infection].
Chagas disease is associated with several immunological alterations. Although resistance against infection with Trypanosoma cruzi has been shown to be influenced by the immune system, its participation in the development of the disease remains unclear. In this regard, cytokines play a fundamental role since they are involved in the regulation of hemopoiesis, lymphopoiesis and affect the function of all cell types involved in an immune response. Interferon gamma (IFN-gamma) has been extensively involved as a protective lymphokine against T. cruzi. Macrophages activated by IFN-gamma result in the release of reactive oxygen metabolites (ROS) and nitric oxide (NO). On the other hand, interleukin 4 (IL-4), interleukin 10 (IL-10) and transforming growth factor beta (TGF-beta) are able to down-regulate the intracellular control of T. cruzi infection by IFN-gamma-activated macrophages, to inhibit NO release and to down-regulate the activity of the TH1 subset of cells (IFN-gamma producers). While TNF-alpha has been implicated in the resistance as well as in the generation of tissue damage, interleukin 6 (IL-6) and interleukin 1 (IL-1) are associated with a variety of alterations in endothelial cell function which may be responsible for the microvascular spasm seen in chagasic myocardiopathy. Several cytokines, including IFN-gamma, IL-1 alpha, IL-6 and TNF-alpha have been shown to modulate the expression of adhesion molecules which participate in inflammatory process by recruitment of lymphocytes into inflammatory sites, contributing to the progression of the local inflammatory reaction in chagasic cardiomyopathy. Thus, it has been shown that acute infection with different strains of T. cruzi induced enhanced expression of ICAM-1 not only on infiltrating leukocytes but also on sarcolemma of cardiocytes and paralleled the production of proinflammatory cytokines. Experimental infection with T. cruzi induces cytokine production which in time modulates the resistance against the parasite and probably the development of chronic Chagas disease. Therefore, it can be postulated that an alteration in quantity and/or quality of cytokine production may be the cause of chronic Chagas disease.
Laucella
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SA
Instituto Nacional de Chagas Dr. Mario Fatala Chaben, Buenos Aires, Argentina.
Rottenberg
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ME
de Titto
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EH
D000818:Animals; D002598:Chagas Cardiomyopathy / Q000276:immunology / Q000473:pathology; D014355:Chagas Disease / Q000276:immunology* / Q000473:pathology; D016207:Cytokines / Q000502:physiology*; D004730:Endothelium, Vascular / Q000473:pathology; D006801:Humans; D007113:Immunity, Innate; D008262:Macrophage Activation; D009569:Nitric Oxide / Q000096:biosynthesis; D006377:T-Lymphocytes, Helper-Inducer / Q000145:classification / Q000276:immunology; D014349:Trypanosoma cruzi / Q000276:immunology*
D016207:Cytokines; D009569:Nitric Oxide
Papel de las citoquinas en la resistencia y patología durante la infección con Trypanosoma cruzi.