Aspectos fisiopatológicos e imunológicos da confecção experimental por Ascaris suum e Plasmodium berghei NK65

Detalhes bibliográficos
Ano de defesa: 2019
Autor(a) principal: Flaviane Vieira Santos
Orientador(a): Não Informado pela instituição
Banca de defesa: Não Informado pela instituição
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 Parasitologia
UFMG
Programa de Pós-Graduação: Não Informado pela instituição
Departamento: Não Informado pela instituição
País: Não Informado pela instituição
Palavras-chave em Português:
Link de acesso: http://hdl.handle.net/1843/35418
Resumo: Ascaridosis and malaria are parasitic diseases prevalent in tropical and subtropical regions, and frequently sharing overlapping endemic areas, which contributes to high rates of morbidity and mortality in areas with poor sanitary conditions. Despite several studies suggesting possible influence of helminth infections on the morbidity of malaria, mostly results are still contradictory and inconclusive. The immune response in ascaridosis is characterized by the involvement of IL-5, IL-4 and IL-13 cytokines, and the IL-10 and TGF-β regulatory factors in addition to circulating levels of total IgE. On the other hand, the protective immune response against malaria is mediated by the production of cytokines IFN-γ and TNF-α. Therefore, helminth coinfection might has a strong potential to influence the progress of protozoan infections. The present work aimed to describe the pathophysiological and immunobiological features of the experimental coinfection of Ascaris suum and Plasmodium berghei NK65. Our results demonstrate that coinfection promote significant changes in the kinetic larval migration, resulting in a higher helminthic parasite burden. Furthermore, it was evidenced a presence of hepatic and pulmonary lesions, which led to the impairment of the physiological function. Finally, the coinfection elicited in downregulation of Th1, Th17, Th2 and Treg responses, which reflected on morbidity and mortality of animals.