Previous Article | Next Article ![]()
Infection and Immunity, March 2000, p. 1231-1234, Vol. 68, No. 3
Department of
Microbiology1 and Department of
Pathology,3 Colorado State University, Fort
Collins, Colorado 80523, and Laboratory of Host Defense,
National Institute of Allergy and Infectious Diseases, National
Institutes of Health, Bethesda, Maryland 208922
Received 19 October 1999/Returned for modification 17 November
1999/Accepted 30 November 1999
Mycobacterium tuberculosis is an important respiratory
pathogen the growth of which is controlled primarily by
cytokine-activated macrophages. One of the principal mediators of this
control is nitric oxide; however, superoxide has recently been shown to
be protective in systemic mycobacterial infections. To determine whether superoxide is important in controlling M. tuberculosis during primary pulmonary infection, mice lacking the
cytosolic p47phox gene (which is essential for
effective superoxide production by the NADPH oxidase) were infected
aerogenically. The lack of superoxide during an aerosol infection with
M. tuberculosis resulted in a significant increase in
bacterial growth over the early period of infection. Once
antigen-specific gamma interferon-producing lymphocytes were detected
in the draining lymph nodes, however, bacterial growth in the lung
stopped. One interesting consequence of the lack of superoxide was an
increase in neutrophilic infiltrates within the granuloma. This may be
a consequence of increased tissue damage due to more rapid bacterial
growth or may reflect a role for superoxide in controlling inflammation.
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
Transient Loss of Resistance to Pulmonary
Tuberculosis in p47phox
/
Mice
*
Corresponding author. Mailing address: Department of
Microbiology, Colorado State University, 200 West Lake, Fort Collins, CO 80523. Phone: (970) 491-2833. Fax: (970) 491-1815. E-mail: acooper{at}cvmbs.colostate.edu.
This article has been cited by other articles:
| J. Bacteriol. | J. Virol. | Eukaryot. Cell |
|---|
| Microbiol. Mol. Biol. Rev. | Clin. Vaccine Immunol. | All ASM Journals |
|---|