Interferon-γ induced nitric oxide mediates in vitro neuronal damage by Trypanosoma cruzi-infected macrophages

摘要: Neuronal lesions and peripheral denervation in Chagas' disease are related to local inflammation; however, the pathogenic mechanisms of neuronal heart megavisceras still unclear. We investigated involvement nitric oxide (NO) on lesion co-cultures neurons macrophages. Trypanosoma cruzi-infected interferon-γ (IFN-γ)-activated wild-type (WT) macrophages showed significant reduction both survival neurite density. These findings correlated with levels NO expression inducible synthase (iNOS). Accordingly, rate was recovered control by treatment cultures iNOS inhibitor, aminoguanidine. Moreover, neither nor density affected when were harvested from iNOS-deficient mice. results demonstrate that iNOS-derived is major molecule involved damage mechanism our vitro model neuropathology.