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* Department of Microbiology and Immunology, University of Arkansas for Medical Sciences, Little Rock, AR 72205;
Boston University School of Medicine, Boston, MA 02118;
Milstead Pathology PC, Atlanta, GA 30012;
Department of Pediatrics, University of Arkansas for Medical Sciences, Little Rock, AR 72205; and
¶ Arkansas Children’s Hospital Research Institute, Little Rock, AR 72202
Chlamydia trachomatis is the most prevalent sexually transmitted bacterial infection in the world. In women, genital infection can cause endometritis and pelvic inflammatory disease with the severe sequelae of ectopic pregnancy or infertility. Chlamydia sp. do not damage tissues directly, but induce an injurious host inflammatory response at the infected site. In the murine model of genital disease with Chlamydia muridarum, TLR2 plays a role in both early production of inflammatory mediators and development of chronic oviduct pathology. We report the results of studies with plasmid-cured C. muridarum mutants that retain the ability to infect the murine genital tract, but fail to cause disease in the oviduct. These mutants do not stimulate TLR2-dependent cytokine production in mice, nor in innate immune cells or epithelial cells in vitro. They induce an effective Th1 immune response, with no evidence for Th1-immune-mediated collateral tissue damage. Furthermore, mice previously infected with the plasmid-deficient strains are protected against oviduct disease upon challenge with virulent C. muridarum. If plasmid-cured derivatives of human C. trachomatis biovars exhibit similar phenotypic characteristics, they have the potential to serve as vaccines to prevent human disease.
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
1 This work was supported by Horace C. Cabe Foundation, Bates-Wheeler Foundation, Arkansas Children’s Hospital Research Institute, and University of Arkansas Medical Sciences. R.R.I. is supported by National Institutes of Health/National Institute of Allergy and Infectious Diseases AI064749.
2 Address correspondence and reprint requests to Dr. Catherine M. O’Connell, Department of Pediatrics (Infectious Diseases Section), Children’s Hospital of Pittsburgh of University of Pittsburgh Medical Center, 3705 Fifth Avenue, Pittsburgh, PA 15213. E-mail address: Catherine.O'Connell{at}chp.edu
3 Abbreviations used in this paper: PRR, pattern recognition receptor; IFU, inclusion-forming unit; KO, knockout; MOI, multiplicity of infection; ShEC, immortalized ectocervical epithelial cell line.
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  Z. Li, D. Chen, Y. Zhong, S. Wang, and G. Zhong The Chlamydial Plasmid-Encoded Protein pgp3 Is Secreted into the Cytosol of Chlamydia-Infected Cells Infect. Immun., August 1, 2008; 76(8): 3415 - 3428. [Abstract] [Full Text] [PDF]
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