Abstract
Tuberculosis is a severe contagious disease caused by Mycobacterium tuberculosis (Mtb). To develop new vaccines and medicine against TB, there is an urgent need to provide insights into the mechanisms by which Mtb induces tuberculosis. In this study, we found that secreted Mtb virulence factor MptpB significantly enhanced the survival of H37Rv in macrophages. MptpB suppressed the production of iNOS, the expression of inflammatory factors IL-1β and IL-6, as well as the apoptosis of the macrophage in Mtb infected RAW264.7 cells. Mechanism investigation showed that MptpB simultaneously hampered the NF-κB and MAPK signal pathways, evidenced by its blocking of p65, IKKα, Erk1/2, and p38 phosphorylation induced by Mtb infection. MptpB also inhibited host cell p53 expression. The results demonstrated that MptpB contributed to the survival of H37Rv by inhibiting host inflammatory responses and apoptosis through impeding the NF-κB and MAPK signal pathways and p53 expression in the macrophage.
Highlights
Tuberculosis is a chronic contagious disease caused by Mycobacterium tuberculosis that threatens human life
Macrophages are primary innate immune cells that contribute to the host immunity against mycobacterial infections by recognizing, engulfing, and eventually killing invasive Mycobacterium tuberculosis (Mtb) (Hmama et al, 2015; Shen et al, 2016; Liu et al, 2017)
Recent studies have shown that macrophage is a main sanctuary to mycobacteria as it establishes various mechanisms to respond to the invasion of pathogens as well as regulate host fate (Killick et al, 2013; Dey and Bishai, 2014; Xu et al, 2014; Arbués et al, 2016; Liu et al, 2017)
Summary
Tuberculosis is a chronic contagious disease caused by Mycobacterium tuberculosis that threatens human life. Mtb elicits numerous immune evasion mechanisms to favor its survival and proliferation and eventually results in formation of tuberculosis (Stokes and Waddell, 2009). Several such mechanisms have been discovered, including inhibiting the formation of phagolysosome, avoiding the toxic effects of reactive nitrogen species, affecting cell proliferation or migration, and interfering with antigen presentation (Kang et al, 2005; Reusch et al, 2006; Vandal et al, 2009; Torrelles and Schlesinger, 2010; Liu et al, 2017). Our study on the mechanisms how Mtb virulence factor MptpB induces immune evasion will provide basis for a better treatment strategy of tuberculosis
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