Salmonella Typhimurium secondary infection induced macrophages apoptosis NO-dependent during Mycobacterium neoaurum infection

Abstract

Mycobacterium neoaurum (M. neoaurum) and Salmonella Typhimurium (S. Typhimurium) are important zoonotic pathogens, and both are intracellular bacteria, which can induce cellular immunity. Coinfection is prevalent worldwide, even more prevalent than single infection. This study aimed to investigate the effect of M. neoaurum/S. Typhimurium coinfection on the percentage property of C57BL/6 mice regulatory T cells (Tregs) and the immune activity of RAW264.7 cells. The secretion of TNF-α, IFN-γ, IL-1β, IL-12 and iNOS in RAW264.7 cells was determined by ELISA. The expression of CD40+ , CD80+ and CD86+ costimulatory molecules on the surface of macrophages was analyzed by flow cytometry. A Nitric oxide (NO) assay was used to detect the production of NO in RAW264.7 cells. The apoptosis of RAW264.7 cells was detected by flow cytometry. The results showed that macrophage expressed a large number of cytokines and surface costimulatory molecules to enhance immune activity. S. Typhimurium secondary infection significantly increased the expression of iNOS and generation of NO, and M. neoaurum/S. Typhimurium-induced apoptosis was NO-dependent. Our data provide a theoretical basis for secondary infections by other pathogens after Nontuberculous Mycobacterium (NTM) infection, and lay a foundation for further research.