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Infection and Immunity, July 2009, p. 3080-3089, Vol. 77, No. 7
0019-9567/09/$08.00+0     doi:10.1128/IAI.00611-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Distinct Roles of CD28- and CD40 Ligand-Mediated Costimulation in the Development of Protective Immunity and Pathology during Chlamydia muridarum Urogenital Infection in Mice{triangledown}

Lili Chen,1,3,{dagger} Wen Cheng,1,4,{dagger} Pooja Shivshankar,1,{dagger} Lei Lei,1 Xiaoyun Zhang,1 Yimou Wu,3 I-Tien Yeh,2 and Guangming Zhong1*

Departments of Microbiology and Immunology,1 Pathology, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, San Antonio, Texas 78229,2 Department of Pathogen Biology, University of South China, 28 Changshen Rd., Hengyang,3 Department of Immunology, Xiangya Medical School, The Central South University, 168 Tongzipo Rd., Changsha, Hunan, China4

Received 19 May 2008/ Returned for modification 28 July 2008/ Accepted 20 April 2009

Infection with Chlamydia muridarum in the mouse urogenital tract can induce both protective immunity and inflammatory pathologies, which has been used as a model for understanding the immune and pathogenic mechanisms of C. trachomatis infection. We compared the roles of CD28- and CD40 ligand (CD40L)-mediated costimulation in C. muridarum infection. Mice with CD28 or CD80/CD86 gene knockout (KO) displayed an infection course similar to that of wild-type mice during both primary and secondary infection, suggesting that CD28-mediated costimulation is not required for protection against C. muridarum infection. However, mice deficient in CD40L or CD40 displayed a prolonged infection course after primary or secondary infection, suggesting that CD40-CD40L costimulation plays an essential role in the development of anti-C. muridarum immunity. Interestingly, the CD28- or CD80/CD86-deficient mice displayed significantly lower levels of inflammatory pathologies in the upper genital tracts after primary infection, although the attenuation in inflammation was no longer significant during secondary infection. However, the CD40L or CD40 KO mice developed inflammatory pathologies as severe as those in wild-type mice following either primary or secondary infection despite the obvious deficits in adaptive immunity in these KO mice. The resistance of CD28 or CD80/CD86 KO mice to chlamydial infection correlated with production of gamma interferon, while the development of inflammatory pathologies in CD40L or CD40 KO mice correlated with the production of other proinflammatory cytokines in mouse urogenital tracts during the early stages of the infection. These observations together suggest that C. muridarum-induced protective immunity and inflammatory pathologies can be mediated by distinct costimulatory signals.

* Corresponding author. Mailing address: Department of Microbiology and Immunology, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Dr., San Antonio, TX 78229. Phone: (210) 567-1169. Fax: (210) 567-0293. E-mail: zhongg{at}uthscsa.edu

{triangledown} Published ahead of print on 27 April 2009.

Editor: S. R. Blanke

{dagger} L.C., W.C., and P.S. contributed equally to this study.

Infection and Immunity, July 2009, p. 3080-3089, Vol. 77, No. 7
0019-9567/09/$08.00+0     doi:10.1128/IAI.00611-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





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