This Article Full Text (PDF) Other Versions of this Article: IAI.01525-06v1 75/3/1280    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Derbigny, W. A. Articles by Johnson, R. M. Search for Related Content PubMed PubMed Citation Articles by Derbigny, W. A. Articles by Johnson, R. M.

 Previous Article  |  Next Article 

Infect. Immun. doi:10.1128/IAI.01525-06
Copyright (c) 2006, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Chlamydia muridarum Infection Elicits an IFN- Response in Murine Oviduct Epithelial Cells Dependent on IRF3 and TRIF

Department of Medicine, Department of Microbiology Immunology, Department of Biostatistics, Indiana University School of Medicine, Indianapolis, Indiana 46202

^* To whom correspondence should be addressed. Email: raymjohn{at}iupui.edu.

	Abstract

Chlamydia trachomatis is the most common sexually transmitted bacterial infection in the United States. Utilizing cloned murine oviduct epithelial cell lines, we previously identified TLR2 as the principal epithelial pattern recognition receptor (PRR) for infection-triggered release of the acute inflammatory cytokines IL-6 and GM-CSF. The infected oviduct epithelial cell lines also secreted the immunomodulatory cytokine IFN- in a largely MyD88-independent manner. Though TLR3 was the only IFN- production-capable TLR expressed by the oviduct cell lines, we were not able to determine whether TLR3 was responsible for IFN- production because the epithelial cells were unresponsive to the TLR3 ligand poly I:C, and siRNA techniques were ineffective at knocking down TLR3 expression. To further investigate the potential role of TLR3 in infected epithelial cell secretion of IFN-, we examined the roles of its downstream signaling molecules TRIF and 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- production. These data implicate TLR3, or an unknown PRR utilizing TRIF, as the source of IFN- production by Chlamydia-infected oviduct epithelial cells.