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Infection and Immunity, April 1999, p. 1606-1613, Vol. 67, No. 4
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Immunity to Chlamydia trachomatis Mouse Pneumonitis Induced by Vaccination with Live Organisms Correlates with Early Granulocyte-Macrophage Colony-Stimulating Factor and Interleukin-12 Production and with Dendritic Cell-Like Maturation

Dongji Zhang, Xi Yang, Hang Lu, Guangming Zhong, and Robert C. Brunham*

Department of Medical Microbiology, University of Manitoba, Winnipeg, Canada

Received 2 October 1998/Returned for modification 17 November 1998/Accepted 13 January 1999

As is true for other intracellular pathogens, immunization with live Chlamydia trachomatis generally induces stronger protective immunity than does immunization with inactivated organism. To investigate the basis for such a difference, we studied immune responses in BALB/c mice immunized with viable or UV-killed C. trachomatis mouse pneumonitis (MoPn). Strong, acquired resistance to C. trachomatis infection was elicited by immunization with viable but not dead organisms. Immunization with viable organisms induced high levels of antigen-specific delayed-type hypersensitivity (DTH), gamma interferon production, and immunoglobulin A (IgA) responses. Immunization with inactivated MoPn mainly induced interleukin-10 (IL-10) production and IgG1 antibody without IgA or DTH responses. Analysis of local early cytokine and cellular events at days 3, 5, and 7 after peritoneal cavity immunization showed that high levels of granulocyte-macrophage colony-stimulating factor and IL-12 were detected with viable but not inactivated organisms. Furthermore, enrichment of a dendritic cell (DC)-like population was detected in the peritoneal cavity only among mice immunized with viable organisms. The results suggest that early differences in inducing proinflammatory cytokines and activation and differentiation of DCs may be the key mechanism underlying the difference between viable and inactivated organisms in inducing active immunity to C. trachomatis infection.

* Corresponding author. Mailing address: Department of Medical Microbiology, University of Manitoba, 543-730 William Ave., Winnipeg, Manitoba R3E OW3, Canada. Phone: (204) 789-3524. Fax: (204) 789-3926. E-mail: Robert_Brunham{at}UManitoba.CA.

Infection and Immunity, April 1999, p. 1606-1613, Vol. 67, No. 4
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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