HIV-1 infection modulates IL-24 expression which contributes to cell apoptosis in vitro

Autor(es)

Strumillo, Scheilla Teixeira ^[1] ; Curcio, Marli Ferreira ^[1] ; de Carvalho, Jr., Fabio Ferreira ^[2] ; Sucupira, MariaCecilia Araripe ^[1] ; Diaz, Ricardo Sobhie ^[1] ; Monteiro, Hugo Pequeno ^[3] ; Ramos Janini, Luiz Mario ^{[4, 1]}

Afiliação do(s) autor(es)

^[1] Univ Fed Sao Paulo, Lab Retrovirol, Disciplina Infectol, Sao Paulo - Brazil

^[2] Hosp Israelita Albert Einstein, Unidade Alphaville, Sao Paulo - Brazil

^[3] Univ Fed Sao Paulo, Lab Sinalizacao Celular, Disciplina Bioquim, Sao Paulo - Brazil

^[4] Univ Fed Sao Paulo, Dept Microbiol Imunol & Parasitol, Disciplina Microbiol, Sao Paulo - Brazil

• Tipo de documento: Artigo Científico
• Fonte: Cell Biology International; v. 43, n. 5, p. 574-579, MAY 2019.
• Citações Web of Science: 0

Resumo

Although interleukin-24 (IL-24) has been extensively explored in the immunopathologies of autoimmune diseases, neoplasms, and infections, its role in HIV-1 infection has not been thoroughly elucidated to date. Therefore, the objective of this study was to evaluate the gene and protein expressions of IL-24 at the initial moments of HIV infection in PBMCs. Due to the pro-apoptotic role of IL-24, we evaluated the protein expression of caspase-3, as well as Annexin V/Propidium Iodide flow cytometry and phosphorylation of ERK, which may induce an apoptotic signal block when phosphorylated. The results of this study demonstrated that HIV-1 infection had an impact on the gene and protein expressions of IL-24 and ERK. Annexin V/Propidium Iodide assay demonstrated decrease in the mechanisms of apoptosis in infected cells after incubation of IL-24 neutralizing antibody. Studies on how HIV-1 regulates IL-24 expression may play a role in characterizing viral persistence mechanisms and designing antiretroviral strategies. (AU)

• Processo FAPESP: 10/07236-1 - Vírus como agentes modificadores do ambiente celular
• Beneficiário: Luiz Mário Ramos Janini
• Modalidade de apoio: Auxílio à Pesquisa - Regular