Poster Presentation (Doctor’s Session)This journal issue contain proceedings of the CongressMycobacterium tuberculosis is an intracellular pathogen and the causative agent of the disease tuberculosis. Macrophages are the major immunocytes to initiate host immunity against mycobacteria. Among the multiple strategies employ by macrophages to defence against mycobacteria, phagocytosis is the first step. Throughphagocytosis, macrophages could not only clear the pathogens from infection sites, but also present antigens derived from the engulfed bacteria to lymphoid cells. c-Myc is a transcription factor that regulates a variety of target genes. It can form a complex with Max and bind to the enhancer box sequences of the promoter to mediate the transcription. Recently, our group revealed that c-Myc has a potential role in regulating the antimicrobial responses in macrophages. Here, we further revealed that c-Myc may play a positive role in phagocytosis and contribute to host defense to mycobacteria. Pretreatment of c-Myc inhibitor, 10058-F4, could significantly reduce the amount of mycobacteria internalised by macrophages. The acidification of phagolysosome in mycobacteria infected macrophages was also inhibited by 10058-F4. Further investigation showed that macrophages phagocytose mycobacteria in a PI3K/Akt independent pathway. And the action of c-Myc inhibitor does not affect the expression levels of Rho family GTPases. However, we found that 10058-F4 could significantly inhibit phorsphorylation of ERK1/2 kinase, which has been indicated to play a role in FcR mediated phagocytosis in macrophage. In conclusion, c-Myc may play a role in phagocytosis of mycobacteria through regulating phorsphorylation of ERK1/2.published_or_final_versio
