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Infection and Immunity, February 2008, p. 515-522, Vol. 76, No. 2
0019-9567/08/$08.00+0     doi:10.1128/IAI.01064-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Caspase-1 Contributes to Chlamydia trachomatis-Induced Upper Urogenital Tract Inflammatory Pathologies without Affecting the Course of Infection{triangledown}

Wen Cheng,1,3 Pooja Shivshankar,1 Zhongyu Li,1,4 Lili Chen,1 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 Departments of Immunology,3 Parasitology, The Central South University, Xiangya Medical School, 168 Tongzipo Rd., Changsha, Hunan 410013, People's Republic of China4

Received 1 August 2007/ Returned for modification 5 September 2007/ Accepted 3 November 2007

Chlamydia trachomatis infection induces inflammatory pathologies in the upper genital tract, potentially leading to ectopic pregnancy and infertility in the affected women. Caspase-1 is required for processing and release of the inflammatory cytokines interleukin-1β (IL-1β), IL-18, and possibly IL-33. In the present study, we evaluated the role of caspase-1 in chlamydial infection and pathogenesis. Although chlamydial infection induced caspase-1 activation and processing of IL-1β, mice competent and mice deficient in caspase-1 experienced similar courses of chlamydial infection in their urogenital tracts, suggesting that Chlamydia-activated caspase-1 did not play a significant role in resolution of chlamydial infection. However, when genital tract tissue pathologies were examined, the caspase-1-deficient mice displayed much reduced inflammatory damage. The reduction in inflammation was most obvious in the fallopian tube tissue. These observations demonstrated that although caspase-1 is not required for controlling chlamydial infection, caspase-1-mediated responses can exacerbate the Chlamydia-induced inflammatory pathologies in the upper genital tract, suggesting that the host caspase-1 may be targeted for selectively attenuating chlamydial pathogenicity without affecting the host defense against chlamydial infection.

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

{triangledown} Published ahead of print on 19 November 2007.

Editor: S. R. Blanke

Infection and Immunity, February 2008, p. 515-522, Vol. 76, No. 2
0019-9567/08/$08.00+0     doi:10.1128/IAI.01064-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.



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