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J. Biol. Chem., Vol. 281, Issue 3, 1652-1659, January 20, 2006

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Localization of TLR2 and MyD88 to Chlamydia trachomatis Inclusions

EVIDENCE FOR SIGNALING BY INTRACELLULAR TLR2 DURING INFECTION WITH AN OBLIGATE INTRACELLULAR PATHOGEN^*

Catherine M. O'Connell, Irina A. Ionova, Alison J. Quayle¶, Alberto Visintin||, and Robin R. Ingalls1

From the Department of Microbiology/Immunology, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205, the Department of Infectious Diseases, Boston Medical Center, Boston University School of Medicine, Boston, Massachusetts 02118, the ^¶Department of Immunology, Microbiology and Parasitology, Louisiana State University Health Sciences Center, New Orleans, Louisiana 70112, and the ^||Department of Infectious Diseases, University of Massachusetts Medical School, Worcester, Massachusetts 01655

Chlamydia trachomatis is an obligate intracellular Gram-negative pathogen and the etiologic agent of significant ocular and genital tract diseases. Chlamydiae primarily infect epithelial cells, and the inflammatory response of these cells to the infection directs both the innate and adaptive immune response. This study focused on determining the cellular immune receptors involved in the early events following infection with the L2 serovar of C. trachomatis.We found that dominant negative MyD88 inhibited interleukin-8 (IL-8) secretion during a productive infection with chlamydia. Furthermore, expression of Toll-like receptor (TLR)-2 was required for IL-8 secretion from infected cells, whereas the effect of TLR4/MD-2 expression was minimal. Cell activation was dependent on infection with live, replicating bacteria, because infection with UV-irradiated bacteria and treatment of infected cells with chloramphenicol, but not ampicillin, abrogated the induction of IL-8 secretion. Finally, we show that both TLR2 and MyD88 co-localize with the intracellular chlamydial inclusion, suggesting that TLR2 is actively engaged in signaling from this intracellular location. These data support the role of TLR2 in the host response to infection with C. trachomatis. Our data further demonstrate that TLR2 and the adaptor MyD88 are specifically recruited to the bacterial or inclusion membrane during a productive infection with chlamydia and provide the first evidence that intracellular TLR2 is responsible for signal transduction during infection with an intracellular bacterium.

Received for publication, September 15, 2005

^* This work was supported by National Institutes of Health Grants AI064749 and AI46613 (to R. R. I.) and Grant AI061972 (to A. J. Q.) and the Research Council of Norway. 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 To whom correspondence should be addressed: Evans Biomedical Research Center, 650 Albany St., Boston, MA 02118. Tel.: 617-414-4778; Fax: 617-414-5280; E-mail: ringalls{at}bu.edu.

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