The PGE(2)/IL-10 Axis Determines Susceptibility of B-1 Cell-Derived Phagocytes (B-1CDP) to Leishmania major Infection

• Autor(a) principal: Arcanjo, Angelica F.
• Data de Publicação: 2015
• Outros Autores: LaRocque-de-Freitas, Isabel F., Rocha, Juliana Dutra B., Zamith, Daniel, Costa-da-Silva, Ana Caroline, Nunes, Marise Pinheiro, Mesquita-Santos, Fabio P., Morrot, Alexandre, Filardy, Alessandra A., Mariano, Mario [UNIFESP], Bandeira-Melo, Christianne, DosReis, George A., Decote-Ricardo, Debora, Freire-de-Lima, Celio Geraldo
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Repositório Institucional da UNIFESP
• dARK ID: ark:/48912/0013000015bfn
• DOI: 10.1371/journal.pone.0124888
• Texto Completo: http://dx.doi.org/10.1371/journal.pone.0124888; http://repositorio.unifesp.br/handle/11600/39018

B-1 cells can be differentiated from B-2 cells because they are predominantly located in the peritoneal and pleural cavities and have distinct phenotypic patterns and activation properties. A mononuclear phagocyte derived from B-1 cells (B-1CDP) has been described. As the B-1CDP cells migrate to inflammatory/infectious sites and exhibit phagocytic capacity, the microbicidal ability of these cells was investigated using the Leishmania major infection model in vitro. the data obtained in this study demonstrate that B-1CDP cells are more susceptible to infection than peritoneal macrophages, since B-1CDP cells have a higher number of intracellular amastigotes forms and consequently release a larger number of promastigotes. Exacerbated infection by Leishmania major required lipid bodies/PGE(2) and IL-10 by B-1CDP cells. Both infection and the production of IL-10 were decreased when PGE(2) production was blocked by NSAIDs. the involvement of IL-10 in this mechanism was confirmed, since B-1CDP cells from IL-10 KO mice are more competent to control Leishmania major infection than cells from wild type mice. These findings further characterize the B-1CDP cells as an important mononuclear phagocyte that plays a previously unrecognized role in host responses to Leishmania major infection, most likely via PGE(2)-driven production of IL-10.