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Infection and Immunity, March 2007, p. 1280-1290, Vol. 75, No. 3
0019-9567/07/$08.00+0     doi:10.1128/IAI.01525-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

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

Wilbert A. Derbigny,1,2 Soon-Cheol Hong,2 Micah S. Kerr,1 M'hamed Temkit,3 and Raymond M. Johnson1*

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.

* Corresponding author. Mailing address: Division of Infectious Diseases, Department of Medicine, Indiana University School of Medicine, 545 Barnhill Dr., #435, Indianapolis, IN 46202. Phone: (317) 278-6968. Fax: (317) 274-1587. E-mail: raymjohn{at}iupui.edu.

{triangledown} Published ahead of print on 18 December 2006.

Editor: R. P. Morrison

Infection and Immunity, March 2007, p. 1280-1290, Vol. 75, No. 3
0019-9567/07/$08.00+0     doi:10.1128/IAI.01525-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



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