Abstract
To understand the role of NF-kappaB in the development of murine tuberculosis in vivo, NF-kappaB p50 knockout mice were infected with Mycobacterium tuberculosis by placing them in the exposure chamber of an airborne-infection apparatus. These mice developed multifocal necrotic pulmonary lesions or lobar pneumonia. Compared with the levels in wild-type mice, pulmonary inducible nitric oxide synthase, interleukin-2 (IL-2), gamma interferon, and tumor necrosis factor alpha mRNA levels were significantly low but expression of IL-10 and transforming growth factor beta mRNAs were within the normal ranges. The pulmonary IL-6 mRNA expression level was higher. Therefore, NF-kappaB and its interaction with host cells play an important role in the pathogenesis of tuberculosis.
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