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Infection and Immunity, June 2002, p. 3234-3248, Vol. 70, No. 6
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.6.3234-3248.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Differences in Innate Immune Responses (In Vitro) to HeLa Cells Infected with Nondisseminating Serovar E and Disseminating Serovar L2 of Chlamydia trachomatis

Sophie Dessus-Babus,1 Toni L. Darville,2 Francis P. Cuozzo,1 Kaethe Ferguson,1 and Priscilla B. Wyrick1*

Department of Microbiology, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, Tennessee,1 Department of Microbiology and Immunology, University of Arkansas for Medical Sciences, Little Rock, Arkansas2

Received 10 December 2001/ Returned for modification 13 February 2002/ Accepted 7 March 2002

The inflammatory response associated with Chlamydia trachomatis genital infections is thought to be initiated by the release of proinflammatory cytokines from infected epithelial cells. This study focuses on the interactions between C. trachomatis-infected HeLa cells and immune cells involved in the early stages of infection, i.e., neutrophils and macrophages. First, we showed that the expression of interleukin-11 (IL-11), an anti-inflammatory cytokine mainly active on macrophages, was upregulated at the mRNA level in the genital tracts of infected mice. Second, incubation of differentiated THP-1 (dTHP-1) cells or monocyte-derived macrophages (MdM) with basal culture supernatants from C. trachomatis serovar E- or serovar L2-infected HeLa cells resulted in macrophage activation with a differential release of tumor necrosis factor alpha (TNF-{alpha}) and upregulation of indoleamine 2,3-deoxygenase (IDO) but not of Toll-like receptor 2 and 4 mRNA expression. Third, coculture of infected HeLa cells with dTHP-1 cells resulted in a reduction in chlamydial growth, which was more dramatic for serovar E than for L2 and which was partially reversed by the addition of anti-TNF-{alpha} antibodies for serovar E or exogenous tryptophan for both serovars but was not reversed by the addition of superoxide dismutase or anti-IL-8 or anti-IL-1ß antibodies. A gamma interferon-independent IDO mRNA upregulation was also detected in dTHP-1 cells from infected cocultures. Lastly, with a two-stage coculture system, we found that (i) supernatants from neutrophils added to the apical side of infected HeLa cell cultures were chlamydicidal and induced MdM to express antichlamydial activity and (ii) although polymorphonuclear leukocytes released more proinflammatory cytokines in response to serovar E- than in response to L2-infected cells, MdM were strongly activated by serovar L2 infection, indicating that the early inflammatory response generated with a nondisseminating or a disseminating strain is different.

* Corresponding author. Mailing address: Department of Microbiology, Box 50759, VA#1-Rm. 1-41, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, TN 37684. Phone: (423) 439-8079. Fax: (423) 439-8044. E-mail: pbwyrick{at}access.etsu.edu.

Editor: R. N. Moore

Infection and Immunity, June 2002, p. 3234-3248, Vol. 70, No. 6
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.6.3234-3248.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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