Yamada H, Mizuno S, Reza-Gholizadeh M, Sugawara I
Department of Molecular Pathology, The Research Institute of Tuberculosis, Tokyo 204-0022, Japan.
Infect Immun. 2001 Nov;69(11):7100-5. doi: 10.1128/IAI.69.11.7100-7105.2001.
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.
为了解核因子-κB(NF-κB)在小鼠体内结核分枝杆菌感染发展过程中的作用,将NF-κB p50基因敲除小鼠置于空气传播感染装置的暴露室中,使其感染结核分枝杆菌。这些小鼠出现了多灶性坏死性肺部病变或大叶性肺炎。与野生型小鼠相比,肺诱导型一氧化氮合酶、白细胞介素-2(IL-2)、γ干扰素和肿瘤坏死因子α的mRNA水平显著降低,但IL-10和转化生长因子β的mRNA表达在正常范围内。肺IL-6 mRNA表达水平较高。因此,NF-κB及其与宿主细胞的相互作用在结核病发病机制中起重要作用。