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Infection and Immunity, March 2008, p. 942-951, Vol. 76, No. 3
0019-9567/08/$08.00+0     doi:10.1128/IAI.01313-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Intracellular Interleukin-1{alpha} Mediates Interleukin-8 Production Induced by Chlamydia trachomatis Infection via a Mechanism Independent of Type I Interleukin-1 Receptor{triangledown}

Wen Cheng,1 Pooja Shivshankar,2 Youmin Zhong,2 Ding Chen,2 Zhongyu Li,3 and Guangming Zhong2*

Department of Microbiology and Immunology, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, San Antonio, Texas 78229,2 Departments of Immunology,1 Parasitology, The Central South University, Xiangya Medical School, 168 Tongzipo Rd., Changsha, Hunan 410013, The People's Republic of China3

Received 27 September 2007/ Returned for modification 8 November 2007/ Accepted 3 December 2007

Chlamydia trachomatis infection induces a wide array of inflammatory cytokines and chemokines, which may contribute to chlamydia-induced pathologies. However, the precise mechanisms by which Chlamydia induces cytokines remain unclear. Here we demonstrate that the proinflammatory cytokine interleukin-1{alpha} (IL-1{alpha}) plays an essential role in chlamydial induction of the chemokine IL-8. Cells deficient in IL-1{alpha} expression or IL-1{alpha}-competent cells treated with IL-1{alpha}-specific small interfering RNA failed to produce IL-8 in response to chlamydial infection. However, neutralization of extracellular IL-1{alpha} or blockade of or deficiency in type I IL-1 receptor (IL-1RI) signaling did not affect chlamydial induction of IL-8 in cells capable of producing IL-1{alpha}. These results suggest that IL-1{alpha} can mediate the chlamydial induction of IL-8 via an intracellular mechanism independent of IL-1RI, especially during the early stage of the infection cycle. This conclusion is further supported by the observations that expression of a transgene-encoded full-length IL-1{alpha} fusion protein in the nuclei enhanced IL-8 production and that nuclear localization of chlamydia-induced precursor IL-1{alpha} correlated with chlamydial induction of IL-8. Thus, we have identified a novel mechanism for chlamydial induction of the chemokine IL-8.

* 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 17 December 2007.

Editor: J. B. Bliska

Infection and Immunity, March 2008, p. 942-951, Vol. 76, No. 3
0019-9567/08/$08.00+0     doi:10.1128/IAI.01313-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.



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