IL-1β Expression Was Induced By Mycoplasma Bovis-derived LAMPs Via MAPK Signaling Pathway

The structures of lipid-assocoated membrane proteins(LAMPs) of M.bovis is similar to the bacterial lipid protein, and works with cell surface receptors, stimulating the immune response of the host. Innate immune response is an important factor against the outside pathogens.Cytokines produced in the course of immune response, it is an important factors for killing pathogens directly recruit other immune cells. In our previous study, we indicated M.bovis LAMPs activate NF-κB signaling pathway by TLR2 receptor. Whether M.bovis LAMPs can activate the MAPK signaling pathway has not been reported.Mitogen-activate protain kinase(MAPK) signaling pathway is a classical signal transduction pathway, and plays an important role in innate immune. TLRs are type I trasnmembrane proteins indenifying the conservative structure of pathogenic microbes in the process of innate immunity. Myeloid differentiation factor 88(MyD88) dependent pathway of MyD88 signaling pathway is the TLR receptor family signaling pathways. TLR1 and TLR2 are in the cell membrane surface. IL-1β as an important inflammatory cytokine, is one of factors which induced immune and inflammatory responses. IL-1β upregulated by the infection of pathogen, is confirmed to be affected by NF-Kappab and MAPK signaling pathways.In order to explore the molecular mechanism of IL-1β expression in EBL cells induced by lipid-associated membrane proteins(LAMPs) of Mycoplasma bovis activating the MAPK Signaling pathway, we investigate the expression kinetics of IL-1β in M.bovis-derived LAMP-stimulated EBL cells and found that M.bovis-derived LAMP stimulation induced IL-1β expression. Further study indicated that p38 MAPK; ERK and JNK MAPK signaling pathways play important roles in M.bovis-derived LAMPs induced IL-1β expression in EBL cells. The overexpression of Toll-like receptor 2(TLR2) and Toll-like receptor 1(TLR1) increased IL-1β expression during LAMPs stimulation. EBL cells incubated by antibody, IL-1β decreased by M.bovis-derived LAMPs stimulated EBL cells. Further study indicated that TLR adaptor myeloid differentiation primary response gene 88(MyD88) and IRAK4 have important roles in IL-1β induction during LAMPs stimulation. Using the commercial ELISA kit for detection of IL-1β protein level was consistent with quantitative results of mRNA level. These results demonstrated that M.bovis-derived LAMPs stimulate EBL cell IL-1β expression through MAPK signaling pathway via TLR2, TLR1, MyD88 and IRAK4.