B-1 cells modulate the murine macrophage response to infection.

AIM

To investigate the modulatory effect of B-1 cells on murine peritoneal macrophages infected with () .

METHODS

Peritoneal macrophages obtained from BALB/c and BALB/c XID mice were infected with 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 (PGE) were determined using a PGE 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 PGE-neutralizing drugs inhibited PGE 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 .

RESULTS

We report that B-1 cells promote the growth of 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 -infected macrophages. Furthermore, the increased secretion of IL-10 was attributed to the presence of the lipid mediator PGE in supernatants of -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 -infected macrophages when the B-1 cells were isolated from IL-10 knockout mice.

CONCLUSION

Our results show that elevated levels of PGE and IL-10 produced by B-1 cells increase growth, as indicated by the number of parasites in cell cultures.