RNA expression profiling of macrophages stimulated with Treponema pallidum

Syphilis is a sexually transmitted disease caused by Treponema pallidum (TP) infection. The incidence of syphilis has increased year by year in recent years, and its prevalence has caused serious public health problems. TP can invade the skin, mucous membranes, nerves, etc., and cause multiple system damage. As an important member of the innate immune response, previous studies have shown that macrophages bind to the TP lipoprotein through the pattern recognition receptor (PRR) on the cell surface to cause self-activation and immune response when infected with TP. Macrophages can participate in the eradication of TP directly through the phagocytosis of TP and the secretion of a large number of inflammatory cytokines. In addition, inflammatory cytokines secreted by macrophages can further stimulate CD4 positive T cells to produce Th1-type cytokines such as IFN-gama and TNF-a and then indirectly eliminate TP. TP infection-induced immune responses can cause tissue damage, and to prevent overwhelming systemic inflammation, macrophages may negatively regulate the inflammatory response upon TP stimulation through related pathways. However, few studies have focused on the negative regulation of the inflammatory response in macrophages during syphilis infection, and the mechanism remains to be further clarified. Our study wanted to explore the mechanisms involved using sequencing data.