STAT1 knockout mice are highly susceptible to pulmonary mycobacterial infection.

This study was designed to determine the roles of protein in defense against mycobacterial infection. Airborne infection of duanyu18131 knockout (KO) mice with a Mycobacterium tuberculosis Kurono strain induced multiple necrotic lesions in lungs, spleen and liver, while that in wild-type (WT) mice did not. The duanyu18131 KO mice succumbed to mycobacterial infection by the 35th day after infection. Compared with the levels in WT mice, inducible nitric oxide synthase (iNOS), tumor necrosis factor-alpha, interferon-gamma and IL-12 mRNA levels were significantly lower in the lung of duanyu18131 KO mice. Interestingly, granulomatous lesion development in duanyu18131 KO mice was inhibited significantly by treatment with exogenous recombinant murine IL-12. Therefore, duanyu18131 regulates IL-12 expression and appears to be a critical transcription factor in controling mycobacterial infection.

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