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Infect Immun, April 1998, p. 1282-1286, Vol. 66, No. 4
0019-9567/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Chlamydial Infection in Inducible Nitric Oxide Synthase Knockout Mice

Joseph U. Igietseme,1,* Linda L. Perry,2 Godwin A. Ananaba,3 Ijindah M. Uriri,1 Omegbhai O. Ojior,1 Shantha N. Kumar,1 and Harlan D. Caldwell2

Department of Microbiology and Immunology, Morehouse School of Medicine, Atlanta, Georgia 303101; Department of Biology, Spelman College, Atlanta, Georgia 303143; and Laboratory of Intracellular Parasites, The Rocky Mountain Laboratories, NIAID/NIH, Hamilton, Montana 598402

Received 21 November 1997/Returned for modification 7 January 1998/Accepted 21 January 1998

Type 1 CD4+-T-cell-mediated immunity is crucial for the resolution of chlamydial infection of the murine female genital tract. Previous studies demonstrating a correlation between CD4+-T-cell-mediated inhibition of chlamydial growth and gamma interferon (IFN-gamma )-mediated induction of nitric oxide synthase suggested a potential role for the nitric oxide (NO) effector pathway in the clearance of Chlamydia from genital epithelial cells by the immune system. To clarify the role of this pathway, the growth levels of Chlamydia trachomatis organisms in normal (iNOS+/+) mice and in genetically engineered mice lacking the inducible nitric oxide synthase (iNOS) gene (iNOS-/- mice) were compared. There was no significant difference in the course of genital chlamydial infections in iNOS+/+ and iNOS-/- mice as determined by recovery of Chlamydia organisms shed from genital epithelial cells. Dissemination of Chlamydia to the spleen and lungs occurred to a greater extent in iNOS-/- than in iNOS+/+ mice, which correlated with a marginal increase in the susceptibility of macrophages from iNOS-/- mice to chlamydial infection in vitro. However, infections were rapidly cleared from all affected tissues, with no clinical signs of disease. The finding of minimal dissemination in iNOS-/- mice suggested that activation of the iNOS effector pathway was not the primary target of IFN-gamma during CD4+-T-cell-mediated control of chlamydial growth in macrophages because previous reports demonstrated extensive and often fatal dissemination of Chlamydia in mice lacking IFN-gamma . In summary, these results indicate that the iNOS effector pathway is not required for elimination of Chlamydia from epithelial cells lining the female genital tract of mice although it may contribute to the control of dissemination of C. trachomatis by infected macrophages.

* Corresponding author. Mailing address: Department of Microbiology and Immunology, Morehouse School of Medicine, 720 Westview Dr., SW, Atlanta, GA 30310. Phone: (404) 752-1596. Fax: (404) 752-1179. E-mail: igietsj{at}msm.edu.




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