| First Author | Sugawara I | Year | 2001 |
| Journal | Am J Pathol | Volume | 158 |
| Issue | 2 | Pages | 361-6 |
| PubMed ID | 11159172 | Mgi Jnum | J:108181 |
| Mgi Id | MGI:3623182 | Doi | 10.1016/S0002-9440(10)63977-6 |
| Citation | Sugawara I, et al. (2001) Disruption of nuclear factor-interleukin-6, a transcription factor, results in severe mycobacterial infection. Am J Pathol 158(2):361-6 |
| abstractText | Nuclear factor-interleukin-6 (NF-IL-6) is one of several nuclear transcription factors (NF-IL-6, NF-kappaB, PU.1, interferon-regulatory factor 1, Egr-1, and Stat-1). NF-IL-6 and NF-kappaB are expressed in macrophages and is induced by bacterial lipopolysaccharides. To evaluate whether NF-IL-6 is required for the inflammatory immune response to mycobacterial infection, in which epithelioid macrophages comprise the leading cell population, we generated NF-IL-6 knockout (KO) mutant mice. Airborne infection of these mice with Mycobacterium tuberculosis strains induced disseminated tuberculosis lacking granuloma formation, although interferon-gamma, tumor necrosis factor-alpha, and interleukin-12 mRNA expression levels were within the normal range compared with those of wild-type mice. Generation of O2- and mycobacterial killing by neutrophils from these mice were impaired severely compared with wild-type mice. We conclude that NF-IL-6 is a critical transcription factor in mycobacterial control as well as in granulocyte-colony stimulating factor induction resulting in neutrophil activation. |
