Abstract
The aim of this study was to evaluate apoptosis and parasite load in the liver and spleen of dogs with visceral leishmaniosis (VL), using immunohistochemistry. Liver and spleen samples from 71 dogs with VL were used. The parasite load in the spleen and liver showed significant difference between organs in infected group (P=0.0219). The density of the parasite load in the spleen (median=2.4) was higher than liver (median=0.8). Immunodetection of apoptotic cells was predominant in lymphocytes and differ between the infected and control group in spleen (P=0.0307) and liver (P=0.0346). There was a significant correlation between apoptosis and parasite load (P = 0.0084; r=0.3104) only in the spleen of the infected group, where it was observed that, when increasing the number of apoptotic cells increases the parasitic load. It was concluded that the liver and spleen of infected dogs presented greater numbers of cells undergoing apoptosis (lymphocytes) than the control group, thus suggesting that this process may be contributing towards the survival of Leishmania in these organs, because lymphocyte in apoptosis did not have the ability to present and recognize the antigen, allowing the survival of the parasite.
Highlights
Visceral leishmaniosis is a zoonosis caused by protozoa of the genus Leishmania
It was concluded that the liver and spleen of infected dogs presented greater numbers of cells undergoing apoptosis than the control group, suggesting that this process may be contributing towards the survival of Leishmania in these organs, because lymphocyte in apoptosis did not have the ability to present and recognize the antigen, allowing the survival of the parasite
The main effector mechanism involved in the protective immune response of dogs infected with Leishmania infantum consists of activation of macrophages by IFN-γ and TNF-α to destroy intracellular amastigotes, via L-arginine and synthesis of nitric oxide (BARBIÉRI, 2006)
Summary
Dogs are considered to be the main reservoirs, outside of the wild environment. They are important for maintaining the epidemiological cycle of the disease, since visceral leishmaniosis is more prevalent in the canine population than in humans (REY, 2001). Human infection is almost always preceded by canine cases, since dogs present greater quantities of parasites on their skins. The presence of systemic lesions is directly related to the host immune response and the evolution of the disease. The main effector mechanism involved in the protective immune response of dogs infected with Leishmania infantum consists of activation of macrophages by IFN-γ and TNF-α to destroy intracellular amastigotes, via L-arginine and synthesis of nitric oxide (BARBIÉRI, 2006)
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