A susceptibilidade de células trofoblásticas humanas (linhagem BeWo) a Toxoplasma gondii é aumentada por interleucina-10 (IL-10) e fator transformador de crescimento beta1 (TGF-β)

• Ano de defesa: 2007
• Autor(a) principal: Barbosa, Bellisa de Freitas
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Federal de Uberlândia; BR; Programa de Pós-graduação em Imunologia e Parasitologia Aplicadas; Ciências Biológicas; UFU
• Palavras-chave em Português: Trofoblasto humano; Imunomodulação; Toxoplasma gondii; Interface maternofetal; Toxoplasmose; Human trophoblast; Immunomodulation; Maternal-fetal interface; CNPQ::CIENCIAS BIOLOGICAS::IMUNOLOGIA
• Link de acesso: https://repositorio.ufu.br/handle/123456789/16719

The present study aimed to investigate the probable causes of BeWo cell susceptibility to Toxoplasma gondii infection in comparison with HeLa cells that served as controls. Both cell types were submitted to different treatments with recombinant citokynes (rIL-10 and rTGF-β1) or their respective antibodies (anti-IL-10 and anti-TGF-β) before or after T. gondii infection. In some experiments, rIFN-γ was added after the parasite infection. Then, cells were fixed, stained and parasites quantified under optical microscopy with regards to intracellular proliferation and infection index (percentage of infected cells per 100 examined cells). Treatments with rIL-10 and rTGF-β1 induced a considerable augment in T. gondii intracellular proliferation and invasion to BeWo but not in Hela cells. Surprisingly, treatment with rIFN-γ caused the same effect, but only the simultaneous treatment with anti-IL-10 and rIFN-γ was able to control the intracellular replication of T. gondii in BeWo cells. Also, anti-TGF-β antibodies showed no influence on the intracellular proliferation or infection index of the parasite to these host cells. These results indicate that BeWo cells may have a different physiologic function in relation to HeLa cells, suggesting that the role of trophoblast cells in maintaining a placental microenvironment that is favorable to pregnancy may facilitate the infection for placental tissues.