Biomaterial Database

[Role of cytokines in resistance and pathology in Trypanosoma cruzi infection]. 1996

S A Laucella, and M E Rottenberg, and E H de Titto

Instituto Nacional de Chagas Dr. Mario Fatala Chaben, Buenos Aires, Argentina.

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.

UI	MeSH Term	Description	Entries
D007113	Immunity, Innate	The capacity of a normal organism to remain unaffected by microorganisms and their toxins. It results from the presence of naturally occurring ANTI-INFECTIVE AGENTS, constitutional factors such as BODY TEMPERATURE and immediate acting immune cells such as NATURAL KILLER CELLS.	Immunity, Native,Immunity, Natural,Immunity, Non-Specific,Resistance, Natural,Innate Immune Response,Innate Immunity,Immune Response, Innate,Immune Responses, Innate,Immunity, Non Specific,Innate Immune Responses,Native Immunity,Natural Immunity,Natural Resistance,Non-Specific Immunity
D008262	Macrophage Activation	The process of altering the morphology and functional activity of macrophages so that they become avidly phagocytic. It is initiated by lymphokines, such as the macrophage activation factor (MAF) and the macrophage migration-inhibitory factor (MMIF), immune complexes, C3b, and various peptides, polysaccharides, and immunologic adjuvants.	Activation, Macrophage,Activations, Macrophage,Macrophage Activations
D009569	Nitric Oxide	A free radical gas produced endogenously by a variety of mammalian cells, synthesized from ARGININE by NITRIC OXIDE SYNTHASE. Nitric oxide is one of the ENDOTHELIUM-DEPENDENT RELAXING FACTORS released by the vascular endothelium and mediates VASODILATION. It also inhibits platelet aggregation, induces disaggregation of aggregated platelets, and inhibits platelet adhesion to the vascular endothelium. Nitric oxide activates cytosolic GUANYLATE CYCLASE and thus elevates intracellular levels of CYCLIC GMP.	Endogenous Nitrate Vasodilator,Mononitrogen Monoxide,Nitric Oxide, Endothelium-Derived,Nitrogen Monoxide,Endothelium-Derived Nitric Oxide,Monoxide, Mononitrogen,Monoxide, Nitrogen,Nitrate Vasodilator, Endogenous,Nitric Oxide, Endothelium Derived,Oxide, Nitric,Vasodilator, Endogenous Nitrate
D002598	Chagas Cardiomyopathy	A disease of the CARDIAC MUSCLE developed subsequent to the initial protozoan infection by TRYPANOSOMA CRUZI. After infection, less than 10% develop acute illness such as MYOCARDITIS (mostly in children). The disease then enters a latent phase without clinical symptoms until about 20 years later. Myocardial symptoms of advanced CHAGAS DISEASE include conduction defects (HEART BLOCK) and CARDIOMEGALY.	Cardiomyopathy, Chagas,Myocarditis, Chagas,Trypanosomiasis, Cardiovascular,Chagas' Cardiomyopathy,Cardiomyopathy, Chagas',Cardiovascular Trypanosomiasis
D004730	Endothelium, Vascular	Single pavement layer of cells which line the luminal surface of the entire vascular system and regulate the transport of macromolecules and blood components.	Capillary Endothelium,Vascular Endothelium,Capillary Endotheliums,Endothelium, Capillary,Endotheliums, Capillary,Endotheliums, Vascular,Vascular Endotheliums
D006377	T-Lymphocytes, Helper-Inducer	Subpopulation of CD4+ lymphocytes that cooperate with other lymphocytes (either T or B) to initiate a variety of immune functions. For example, helper-inducer T-cells cooperate with B-cells to produce antibodies to thymus-dependent antigens and with other subpopulations of T-cells to initiate a variety of cell-mediated immune functions.	Helper Cell,Helper Cells,Helper T Cell,Helper-Inducer T-Lymphocytes,Inducer Cell,Inducer Cells,T-Cells, Helper-Inducer,T-Lymphocytes, Helper,T-Lymphocytes, Inducer,Helper T-Cells,Cell, Helper T,Cells, Helper T,Helper Inducer T Lymphocytes,Helper T Cells,Helper T-Cell,Helper T-Lymphocyte,Helper T-Lymphocytes,Helper-Inducer T-Cell,Helper-Inducer T-Cells,Helper-Inducer T-Lymphocyte,Inducer T-Lymphocyte,Inducer T-Lymphocytes,T Cell, Helper,T Cells, Helper,T Cells, Helper Inducer,T Lymphocytes, Helper,T Lymphocytes, Helper Inducer,T Lymphocytes, Inducer,T-Cell, Helper,T-Cell, Helper-Inducer,T-Cells, Helper,T-Lymphocyte, Helper,T-Lymphocyte, Helper-Inducer,T-Lymphocyte, Inducer
D006801	Humans	Members of the species Homo sapiens.	Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man
D000818	Animals	Unicellular or multicellular, heterotrophic organisms, that have sensation and the power of voluntary movement. Under the older five kingdom paradigm, Animalia was one of the kingdoms. Under the modern three domain model, Animalia represents one of the many groups in the domain EUKARYOTA.	Animal,Metazoa,Animalia
D014349	Trypanosoma cruzi	The agent of South American trypanosomiasis or CHAGAS DISEASE. Its vertebrate hosts are man and various domestic and wild animals. Insects of several species are vectors.	Trypanosoma cruzus,cruzi, Trypanosoma
D014355	Chagas Disease	Infection with the protozoan parasite TRYPANOSOMA CRUZI, a form of TRYPANOSOMIASIS endemic in Central and South America. It is named after the Brazilian physician Carlos Chagas, who discovered the parasite. Infection by the parasite (positive serologic result only) is distinguished from the clinical manifestations that develop years later, such as destruction of PARASYMPATHETIC GANGLIA; CHAGAS CARDIOMYOPATHY; and dysfunction of the ESOPHAGUS or COLON.	Trypanosomiasis, South American,American Trypanosomiasis,Chagas' Disease,Trypanosoma cruzi Infection,Infection, Trypanosoma cruzi,Infections, Trypanosoma cruzi,South American Trypanosomiasis,Trypanosoma cruzi Infections,Trypanosomiasis, American