Effect of prolactin on nitric oxide and interleukin-1 production of murine peritoneal macrophages: role of Ca2+ and protein kinase C.

In vitro treatment of macrophages with prolactin (PRL) was found to increase the production of nitric oxide (NO) and interleukin-1 (IL-1). Production of NO and IL-1 by macrophages got additively enhanced on simultaneous treatment with LPS and PRL. The production of NO was, however, decreased when the macrophages were treated with a combination of PRL and nifedipine, a Ca2+ blocker indicating a role of Ca2+ in the activation of macrophages with PRL. PRL-treated macrophages showed an enhanced translocation of protein kinase C (PKC) from cytosol to the membrane, indicating that PRL activates macrophages via the activation of PKC.