Published online May 26, 2017. doi: 10.4331/wjbc.v8.i2.151
Peer-review started: August 29, 2016
First decision: November 17, 2016
Revised: February 20, 2017
Accepted: March 14, 2017
Article in press: March 15, 2017
Published online: May 26, 2017
Processing time: 264 Days and 1.4 Hours
To investigate the modulatory effect of B-1 cells on murine peritoneal macrophages infected with Leishmania major (L. major) in vitro.
Peritoneal macrophages obtained from BALB/c and BALB/c XID mice were infected with L. major and cultured in the presence or absence of B-1 cells obtained from wild-type BALB/c mice. Intracellular amastigotes were counted, and interleukin-10 (IL-10) production was quantified in the cellular supernatants using an enzyme-linked immunosorbent assay. The levels of the lipid mediator prostaglandin E2 (PGE2) were determined using a PGE2 enzyme immunoassay kit (Cayman Chemical, Ann Arbor, MI), and the number of lipid bodies was quantified in the cytoplasm of infected macrophages in the presence and absence of B-1 cells. Culturing the cells with selective PGE2-neutralizing drugs inhibited PGE2 production and confirmed the role of this lipid mediator in IL-10 production. In contrast, we demonstrated that B-1 cells derived from IL-10 KO mice did not favor the intracellular growth of L. major.
We report that B-1 cells promote the growth of L. major amastigotes inside peritoneal murine macrophages. We demonstrated that the modulatory effect was independent of physical contact between the cells, suggesting that soluble factor(s) were released into the cultures. We demonstrated in our co-culture system that B-1 cells trigger IL-10 production by L. major-infected macrophages. Furthermore, the increased secretion of IL-10 was attributed to the presence of the lipid mediator PGE2 in supernatants of L. major-infected macrophages. The presence of B-1 cells also favors the production of lipid bodies by infected macrophages. In contrast, we failed to obtain the same effect on parasite replication inside L. major-infected macrophages when the B-1 cells were isolated from IL-10 knockout mice.
Our results show that elevated levels of PGE2 and IL-10 produced by B-1 cells increase L. major growth, as indicated by the number of parasites in cell cultures.
Core tip:This original manuscript describes the modulatory effect of B-1 cells on Leishmania major-infected macrophages. We demonstrated the participation of soluble mediators in a co-culture system and characterized prostaglandin E2 and interleukin-10 (IL-10) as key factors involved in increased intracellular parasite replication. We also demonstrated that cell-cell contact is not important. The same effect was not observed when we used B-1 cells from IL-10 knockout mice, as no significant difference in parasite multiplication was observed. Thus, the current manuscript may be of interest for scientists working in the fields of immunoparasitology or immunomodulation.