Fator de Inibição da Migração de Macrófagos (MIF) aumenta a migração e a susceptibilidade de células trofoblasticas extravilosas (HTR8/SVneo) à infecção por Toxoplasma gondii

• Autor(a) principal: Milian, Iliana Claudia Balga
• Data de Publicação: 2017
• Tipo de documento: Dissertação
• Idioma: por
• Título da fonte: Repositório Institucional da UFU
• Texto Completo: https://repositorio.ufu.br/handle/123456789/18191; http://doi.org/10.14393/ufu.di.2017.536
• topic: Imunologia; Citocinas; Células; Toxoplasma gondii; Fator de Inibição da Migração de Macrófagos (MIF); CD44; Fosforilação da ERK1/2; Migração celular; Macrophage Migration Inhibitor Factor (MIF); ER1/2 phosphorylation; Cell migration; CNPQ::CIENCIAS BIOLOGICAS::IMUNOLOGIA

The successful of pregnancy depend about production of many cytokine by extravillous trophoblastic cells migration and the macrophage migration inhibitory (MIF) is important in this process. MIF is a potent cytokine, implicated in several pathological conditions and it is involved in pathogenesis of infections, including toxoplasmosis. Therefore, we investigated the role of MIF in infected HTR8/SVneo cells. The cells were infected with RH strain (2F1) tachyzoites of T. gondii and treated with recombinant MIF (rhMIF) or MIF inhibitor (ISO-1). The cell viability was analyzed by MTT assay, T. gondii intracellular proliferation by colorimetric beta-galactosidase assay, CD44 expression and ERK1/2 phosphorylation by Western blotting and cell migration by scratch assay. The supernatants were collected for MIF production analysis by ELISA. The cells were used to CD44 co-receptor and ERK1/2 phosphorylation analysis. Cellular viability was not changed in infected and/or treated with rhMIF or ISO-1. Cells treated with rhMIF showed high parasite burden, presence of ERK1/2 phosphorylation. In addition, the infection increased extracellular MIF production by HTR8/SVneo cells. In cellular migration assay, ISO-1 treated cells decrease migration compared with rhMIF treated cells. In conclusion, T. gondii infection caused modulation of MIF production and ERK1/2 phosphorylation. Furthermore, MIF was important in the migration of HTR8/SVneo cells, ensuring its permanence in the host cell.