Resumo

Introduction Leptospirosis is an important zoonotic disease spread- worldwide, except in Antarctica. Recently, new outbreaks have been described in humans related to adventure tourism, sporting events, and natural disasters; currently, it presents the possibility of becoming a public health problem. The mechanism by which the causative agent of leptospirosis, Leptospira, activates the immune system has been the main focus of multiple studies, many of which center on the involvement of cytokines. Cellular apoptosis, or programmed cell death, plays an important role in modulating the pathogenesis of many infections.The occurrence of apoptosis following tissue injury is a well-known event in renal disease processesThe cell apoptosis, or programmed cell death, plays an important role in modulating the pathogenesis of many infectious processes. Leptospira interrogans has been considered as a promoter of apoptosis. This investigation aimed to evaluate the occurrence of some apoptosis features induced by Leptospira interrogans serovar Icterohaemorrhagiae infection in BALB/c mice. Materials and Methods The liver, kidney and lungs fragments were evaluated by histopathological and immunohistochemical analysis during 21 days post-infection (dpi). The animals were euthanized on 2, 4, 7, 10, 14 and 21, dpi. Results and Conclusions Histopathologic analysis revealed areas with eosinophilic condensation of nuclear chromatin in kidney and liver tissues but not in lung tissue. The immunostaining with mouse anti-caspase 3 antibody revealed positivity signals observed at 14 and 21 dpi in the renal epithelial cells,significally higer than observed in early dpi. (p=0,025; p< 0,05). Lung sections at 10 and 14 dpi were strong labeled mainly around the alveolar cells Statiscally different from results observed at 7 dpi (p-0,0497); p < 0,05). Liver sections stained positively higher at 14 and 21 dpi, in comparasion to 2 dpi ( p= 0,0069;p< 0,05). Our results suggest that infection of L. interrogans induce in kidney, liver and lung an activation of apoptosis mediated by caspase-3 dependent pathway in later phases of infectious process.