Histopatologia da esquistossomose murina em linhagens mutantes sem mastócitos

• Ano de defesa: 2021
• Autor(a) principal: Clara Lucas Bernardino
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Federal de Minas Gerais; Brasil; ICB - INSTITUTO DE CIÊNCIAS BIOLOGICAS; Programa de Pós-Graduação em Patologia; UFMG
• Palavras-chave em Português: Schistosoma mansoni; Imunopatologia; Esquistossomose; Mastócitos; Modelo murino.; Patologia; Schistosoma mansoni; Esquistossomose; Mastócitos
• Link de acesso: http://hdl.handle.net/1843/50474

In Brazil, schistosomiasis is an endemic and neglected disease, becoming a serious public health problem. The clinical manifestations in the human host are associated with the granulomatous inflammatory reaction to the parasite's eggs, due to the activities of cells that make up the immune system, such as lymphocytes, macrophages, neutrophils and eosinophils. However, the role of mast cells in the immunopathogenesis of schistosomiasis is very little known, showing a knowledge gap that can be mitigated with the use of murine models. In the present study, the histopathology of Schistosoma mansoni infection in a deficient murine model of mast cells was evaluated in the liver, spleen, lung and small and large intestines. In the portal tracts of mast cell deficient mice, greater intensities of inflammatory activities were observed in 34.29% of the mice and less fibrosis in 4.29%, with statistically significant differences in the Control mice, which presented in 4.40% of the mice lower intensity of inflammatory activity and 18.68% higher fibrosis. In the lungs, intestines and spleen, architectural changes and granulomatous inflammatory response were observed around the parasite's eggs in the mast cell deficient group, but without statistically significant differences with the Control group. These results demonstrate that mast cells participate in the immunopathology of schistosomiasis, indicating a probable role that regulates inflammation and induces its resolution by fibrosis. The present study allows new perspectives in the search to understand and elucidate the occurrence of the immune response of schistosomiasis, as well as the participation and performance of mast cells in the disease.