TNFR1 Mediated Apoptosis Is Protective against Mycobacterium avium in Mice.

is an intracellular proliferating pathogen that causes chronic refractory respiratory infection. Although apoptosis induced by has been reported in vitro, the role of apoptosis against infection in vivo remains unclear. Here, we investigated the role of apoptosis in mouse models of infection. Tumor necrosis factor receptor-1 knockout mice (TNFR1-KO) andTNFR2-KO micewere used. (1 × 10 cfu/body) was administered intratracheally to mice. Apoptosis in lungs was detected by terminal deoxynucleotidyl transferase mediated dUTP nick end labeling and lung histology as well as cell death detection kits using BAL fluids. TNFR1-KO mice were susceptible to infection compared with TNFR2-KO and wild type mice based on the bacterial number and lung histology. Higher numbers of apoptotic cells were detected in the lungs of TNFR2-KO and wild-type mice were compared with TNFR1-KO mice. The inhalation of Z-VAD-FMK deteriorated infection compared with vehicle-inhaled controls. Overexpression of Iκ-B alpha by adenovirus vector attenuated infection. Our study showed apoptosis had an important role in innate immunity against in mice. The induction of apoptosis in -infected cells might be a new strategy to control infection.