Trypanosoma cruzi-infected cardiomyocytes produce chemokines and cytokines that trigger potent nitric oxide-dependent trypanocidal activity

The pathogenesis of myocarditis that occurs in Trypanosoma cruzi-infected mice is still poorly understood. Therefore, it is important to know the mediators that trigger leukocyte migration to the heart as well as the cellular source of these possible mediators. In this study, we investigated (1) NO...

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Veröffentlicht in:	Circulation (New York, N.Y.) N.Y.), 2000-12, Vol.102 (24), p.3003-3008
Hauptverfasser:	MACHADO, Fabiana S, MARTINS, Gislaine A, ALIBERTI, Julio C. S, MESTRINER, Fabiola L. A. C, CUNHA, Fernando Q, SILVA, Joao S
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Biological and medical sciences Chagas Cardiomyopathy - immunology Chagas Cardiomyopathy - metabolism Chagas Cardiomyopathy - pathology Chemokines - genetics Chemokines - metabolism Cytokines - genetics Cytokines - metabolism Haplorhini Heart - parasitology Human protozoal diseases Infectious diseases Medical sciences Mice Mice, Inbred BALB C Myocarditis - metabolism Myocarditis - parasitology Myocarditis - pathology Myocardium - metabolism Nitric Oxide - metabolism Nitric Oxide Synthase - metabolism Nitric Oxide Synthase Type II Parasitic diseases Protozoal diseases RNA, Messenger - metabolism Trypanocidal Agents - pharmacology Trypanosoma cruzi - drug effects Trypanosoma cruzi - physiology Trypanosomiasis
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