|
|
||||||||
PATHOGENICITY AND VIRULENCE |
Department of Molecular Pathology, The Research Institute of Tuberculosis, Japan Anti-Tuberculosis Association, 3-1-24 Matsuyama, Kiyose, Tokyo 204-0022, Japan
Correspondence I. Sugawara sugawara{at}jata.or.jp
Received 11 July 2002 Accepted 13 September 2002
This study was designed to determine the roles of STAT proteins in defence against mycobacterial infection. Airborne infection of STAT4 knockout (KO) mice with a Mycobacterium tuberculosis strain induced large granulomas with massive neutrophil infiltration over time, while that in STAT6 KO mice did not. The STAT4 KO mice succumbed to mycobacterial infection by the 80th day after infection. Compared with the levels in wild-type (WT) and STAT6 KO mice, pulmonary inducible nitric oxide synthase, interferon-
, -ß and -
mRNA levels were significantly lower in STAT4 KO mice, but expression of interleukin-2, -6, -12 and -18 mRNAs was slightly higher up to the fifth week after aerial infection. Therefore, STAT4, but not STAT6, appears to be a critical transcription factor in mycobacterial regulation.
This article has been cited by other articles:
![]() |
Y. Maeda, V. Dave, and J. A. Whitsett Transcriptional Control of Lung Morphogenesis Physiol Rev, January 1, 2007; 87(1): 219 - 244. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. C. Deng, X. Zeng, M. Newstead, T. A. Moore, W. C. Tsai, V. J. Thannickal, and T. J. Standiford STAT4 Is a Critical Mediator of Early Innate Immune Responses against Pulmonary Klebsiella Infection J. Immunol., September 15, 2004; 173(6): 4075 - 4083. [Abstract] [Full Text] [PDF] |
||||
![]() |
I. Sugawara, T. Udagawa, and H. Yamada Rat Neutrophils Prevent the Development of Tuberculosis Infect. Immun., March 1, 2004; 72(3): 1804 - 1806. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| INT J SYST EVOL MICROBIOL | J MED MICROBIOL | MICROBIOLOGY | J GEN VIROL | ALL SGM JOURNALS |