- Paper Report
- Open Access
Factors that determine mycobacterial infection
- Undurti Das1
© Biomed Central Ltd 2001
- Received: 13 March 2001
- Accepted: 18 September 2001
- Published: 18 September 2001
- Disseminated tuberculosis, G-CSF, Mycobacterium tuberculosis, NF-IL-6, superoxide
Tuberculosis is a common disease, especially in immunocompromised persons. It is important that we understand the molecular mechanisms by which this organism evades the body's defenses so that new drugs can be developed. Alveolar macrophages are targets of mycobacterial infection. Activated macrophages and secreted lymphokines such as interferon, tumor necrosis factor, and interleukins play a vital role in protection against this infection. The factors that control the production of these lymphokines, and the role of neutrophils in early mycobacterial infection, are not clear. In this study, the authors evaluated the role of nuclear factor interleukin 6 (NF-IL-6) in early mycobacterial infection.
NF-IL-6 knockout mice developed disseminated tuberculosis when infected with Mycobacterium by an airborne route. In comparison with wild-type mice, these animals lack granuloma formation, and show impaired superoxide anion generation and mycobacterial killing by neutrophils. The knockout mice showed normal levels of expression (in the lung tissue and splenocytes) of interferon-?, tumor necrosis factor (TNF), and IL-12, and normal amounts of macrophage nitric oxide production, but expressed less granulocyte-colony stimulating factor (G-CSF) than did wild-type mice. Neutrophil ability to kill the mycobacteria, and both endocytosis and morphology of endosomes, was restored by G-CSF in the knockout mice. Thus, NF-IL-6 may be critical in mycobacterial infection.
NF-IL-6 knockout mice, nitric oxide assay, ELISA, RT-PCR, superoxide anion assay