Parasite load, iNOS and cytokine profiles, and histopathological aspects of Leishmania infantum infection in dogs with different clinical presentations

• Autor(a) principal: Vasconcelos,Tassia Cristina Bello de
• Data de Publicação: 2019
• Outros Autores: Bruno,Sávio Freire, Miranda,Luisa Helena Monteiro de, Conceição-Silva,Fátima, Belo,Vinícius Silva, Figueiredo,Fabiano Borges
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Ciência Rural
• Texto Completo: http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0103-84782019001000501
• topic: visceral leishmaniasis; immunopathology; canine infection; histopathology; canine cytokines

ABSTRACT: Visceral leishmaniasis (VL) is a zoonotic disease with a canine urban reservoir in South America. Dogs from an endemic area within Brazil, which were naturally infected with Leishmania infantum, and those presenting severe clinical (SC), mild, or no clinical (MNC) disease, were evaluated. Parasite load, histopathology, and cytokine and iNOS mRNA expressions were assessed in the spleen and liver in order to determine the potential markers for disease susceptibility or resistance. As a result, dogs with both SC and MNC had high parasite loads; IFN-γ was the most expressive cytokine in both organs, along with IL-6 and IL-4 being detected in the spleen and liver, and IL-10 only in liver. The hepatic tissue presented higher medians for IFN-γ and IL-10, and was the main organ to produce cytokines with hepatic IL-10 suggesting a regulatory follow up. Granulomas were detected in both organs; however, when absent in spleen, they were associated with elevated IL-6 levels, thus highlighting the anti-inflammatory role of IL-6. Microscopic lesions in the spleen were predominantly characterized by an extensively disorganized white pulp and splenic response was suggested as sub optimized. Parasite load, tissue damage, and immunological response may vary in the dogs with similar clinical symptoms, which may not be a good parameter for assessing the animal’s susceptibility to VL.