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Trypanosoma cruzi –Infected Cardiomyocytes Produce Chemokines and Cytokines That Trigger Potent Nitric Oxide–Dependent Trypanocidal Activity
Author(s) -
Fabiana S. Machado,
Gislâine A. Martins,
Júlio Aliberti,
Fabíola Mestriner,
Fernando Q. Cunha,
João S. Silva
Publication year - 2000
Publication title -
circulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.795
H-Index - 607
eISSN - 1524-4539
pISSN - 0009-7322
DOI - 10.1161/01.cir.102.24.3003
Subject(s) - trypanosoma cruzi , nitric oxide , medicine , chemokine , chagas disease , nitric oxide synthase , pharmacology , virology , immunology , inflammation , parasite hosting , world wide web , computer science
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 synthase (NOS) induction, (2) NO synthesis, (3) trypanocidal activity, and (4) chemokine and cytokine mRNA expression by isolated cardiomyocytes infected with T cruzi.

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