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Infection and Immunity, February 2002, p. 844-850, Vol. 70, No. 2
0019-9567/01/$04.00+0     DOI: 10.1128/IAI.70.2.844-850.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Chemokine and Chemokine Receptor Dynamics during Genital Chlamydial Infection

Tesfaye Belay,1 Francis O. Eko,1 Godwin A. Ananaba,2,{dagger} Samera Bowers,2 Terri Moore,1 Deborah Lyn,1 and Joseph U. Igietseme1*

Department of Microbiology, Biochemistry and Immunology, Morehouse School of Medicine, Atlanta, Georgia 30310,1 Department of Biology, Spelman College, Atlanta, Georgia 303142

Received 27 June 2001/ Returned for modification 21 August 2001/ Accepted 23 October 2001

Current design strategies for vaccines against certain microbial pathogens, including Chlamydia trachomatis, require the induction and targeting of specific immune effectors to the local sites of infection known as the mucosal effector sites. Chemokines and their receptors are important mediators of leukocyte trafficking and of the controlled recruitment of specific leukocyte clonotypes during host defense against infections and during inflammation. We analyzed the dynamics of chemokine and chemokine receptor expression in genital mucosae during genital chlamydial infection in a murine model to determine how these molecular entities influence the development of immunity and the clearance of infection. A time course study revealed an increase of up to threefold in the levels of expression of RANTES, monocyte chemotactic protein 1 (MCP-1), gamma-interferon-inducible protein 10 (IP-10), macrophage inflammatory protein 1{alpha} (MIP-1{alpha}), and intercellular adhesion molecule type 1 (ICAM-1) after genital infection with the C. trachomatis agent of mouse pneumonitis. Peak levels of expression of RANTES, MCP-1, and MIP-1{alpha} occurred by day 7 after primary infection, while those of IP-10 and ICAM-1 peaked by day 21. Expression levels of these molecules decreased by day 42 after primary infection, by which time all animals had resolved the infection, suggesting an infection-driven regulation of expression. A rapid upregulation of expression of these molecules was observed after secondary infection. The presence of cells bearing the chemokine receptors CCR5 and CXCR3, known to be preferentially expressed on Th1 and dendritic cells, was also synchronous with the kinetics of immune induction in the genital tract and clearance of infection. Results demonstrated that genital chlamydial infection is associated with a significant induction of chemokines and chemokine receptors that are involved in the recruitment of Th1 cells into the site of infection. Future studies will focus on how selective modulation of chemokines and their receptors can be used to optimize long-term immunity against Chlamydia.

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

Editor: J. D. Clements

{dagger} Present address: Center for Cancer Research and Therapeutic Development, Clark Atlanta University, Atlanta, GA 30314.

Infection and Immunity, February 2002, p. 844-850, Vol. 70, No. 2
0019-9567/01/$04.00+0     DOI: 10.1128/IAI.70.2.844-850.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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