Cu,Zn superoxide dismutase of Mycobacterium tuberculosis contributes to survival in activated macrophages that are generating an oxidative burst.

摘要: Macrophages produce reactive oxygen species and nitrogen that have potent antimicrobial activity. Resistance to killing by macrophages is critical the virulence of Mycobacterium tuberculosis. M. tuberculosis has two genes encoding superoxide dismutase proteins, sodA sodC. SodC a Cu,Zn responsible for only minor portion activity However, lipoprotein binding motif, which suggests it may be anchored in membrane protect from intermediates at bacterial surface. To examine role protecting toxic effects exogenously generated species, we constructed null mutation sodC gene. In this report, show mutant readily killed externally, while isogenic parental unaffected under these conditions. Furthermore, enhanced susceptibility gamma interferon (IFN-γ)-activated murine peritoneal producing oxidative burst products but not activated IFN-γ or respiratory burst-deficient mice. These observations establish contributes resistance against macrophages.