Key result
T cruzi-infected murine cardiomyocytes produce chemokines and cytokines that induce iNOS and potent nitric oxide-dependent trypanocidal activity.
Why the study?
Does Trypanosoma cruzi infection and subsequent cytokine/chemokine production induce NO-dependent trypanocidal activity in mouse cardiomyocytes?
Does Trypanosoma cruzi infection and subsequent cytokine/chemokine production induce NO-dependent trypanocidal activity in mouse cardiomyocytes?
Cardiomyocytes infected with Trypanosoma cruzi produce proinflammatory cytokines and chemokines that trigger NO-dependent trypanocidal activity, which likely contributes to the pathogenesis of chagasic cardiomyopathy.
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Suggests NO-dependent mechanisms contribute to chagasic cardiomyopathy pathogenesis; leaves open human translation and therapeutic targeting.
Machado et al. (2000) studied Trypanosoma cruzi infection. Trypanosoma cruzi infection and cytokine/chemokine addition was evaluated on NO synthase induction, NO synthesis, trypanocidal activity, and chemokine/cytokine mRNA expression. T cruzi-infected murine cardiomyocytes produce chemokines and cytokines that induce iNOS and potent nitric oxide-dependent trypanocidal activity.
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