Activation of macrophage mediated host defense against by L.

Background: The innate immune system plays a crucial role in the initiation and subsequent direction of adaptive immune responses, as well as in the removal of pathogens that have been targeted by an adaptive immune response.

Objective: L. was reported to have immunostimulatory properties that might protect against infectious diseases. However, this possibility has not yet been explored. The present study investigated the protective and immune-enhancing ability of L. against infectious disease and the mechanisms involved.

Design: To investigate the immune-enhancing effects of L., we used a bacterial infection model.

Results And Discussions: The lifespan of mice infected with a lethal dose of (1 × 10 colony forming units - CFU) was significantly extended when they were administered L. Furthermore, L. activated macrophages, monocytes, and neutrophils and induced Th1 cytokines (IL-12, IFN-γ, TNF-α) in mice infected with a sublethal dose (1 × 10 CFU) of . L. significantly stimulated the uptake of bacteria into peritoneal macrophages as indicated by increased phagocytosis. Peritoneal macrophages derived from C3H/HeJ mice significantly inhibited L. induced NO production and TNF-α secretion compared with peritoneal macrophages derived from C3H/HeN mice.

Conclusions: These results suggest that the innate immune activity of L. against bacterial infection in mice occurs through activation of the TLR4 signaling pathway.