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Chlamydia muridarum Infection Elicits a Beta Interferon Response in Murine Oviduct Epithelial Cells Dependent on Interferon Regulatory Factor 3 and TRIF

Department of Medicine,¹ Department of Microbiology Immunology,² Department of Biostatistics, Indiana University School of Medicine, Indianapolis, Indiana 46202³

Received 21 September 2006/ Returned for modification 23 October 2006/ Accepted 11 December 2006

Chlamydia trachomatis is the most common sexually transmitted bacterial infection in the United States. Utilizing cloned murine oviduct epithelial cell lines, we previously identified Toll-like receptor 2 (TLR2) as the principal epithelial pattern recognition receptor (PRR) for infection-triggered release of the acute inflammatory cytokines interleukin-6 and granulocyte-macrophage colony-stimulating factor. The infected oviduct epithelial cell lines also secreted the immunomodulatory cytokine beta interferon (IFN-ß) in a largely MyD88-independent manner. Although TLR3 was the only IFN-ß production-capable TLR expressed by the oviduct cell lines, we were not able to determine whether TLR3 was responsible for IFN-ß production because the epithelial cells were unresponsive to the TLR3 ligand poly(I-C), and small interfering RNA (siRNA) techniques were ineffective at knocking down TLR3 expression. To further investigate the potential role of TLR3 in the infected epithelial cell secretion of IFN-ß, we examined the roles of its downstream signaling molecules TRIF and IFN regulatory factor 3 (IRF-3) using a dominant-negative TRIF molecule and siRNA specific for TRIF and IRF-3. Antagonism of either IRF-3 or TRIF signaling significantly decreased IFN-ß production. These data implicate TLR3, or an unknown PRR utilizing TRIF, as the source of IFN-ß production by Chlamydia-infected oviduct epithelial cells.

Published ahead of print on 18 December 2006.

Editor: R. P. Morrison