This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Johnson, R. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Johnson, R. M.

 Previous Article  |  Next Article 

Infection and Immunity, July 2004, p. 3951-3960, Vol. 72, No. 7
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.7.3951-3960.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Murine Oviduct Epithelial Cell Cytokine Responses to Chlamydia muridarum Infection Include Interleukin-12-p70 Secretion

Raymond M. Johnson*

Division of Infectious Diseases, Indiana University School of Medicine, Indianapolis, Indiana

Received 2 February 2004/ Returned for modification 9 March 2004/ Accepted 31 March 2004

Epithelial cells play an important role in host defense as sentinels for invading microbial pathogens. Chlamydia trachomatis is an intracellular bacterial pathogen that replicates in reproductive tract epithelium. Epithelial cells lining the reproductive tract likely play a key role in triggering inflammation and adaptive immunity during Chlamydia infections. For this report a murine oviduct epithelial cell line was derived in order to determine how epithelial cells influence innate and adaptive immune responses during Chlamydia infections. As expected, oviduct epithelial cells infected by Chlamydia muridarum produced a broad spectrum of chemokines, including CXCL16, and regulators of the acute-phase response, including interleukin-1{alpha} (IL-1{alpha}), IL-6, and tumor necrosis factor alpha. In addition, infected epithelial cells expressed cytokines that augment gamma interferon (IFN) production, including IFN-{alpha}/ß and IL-12-p70. To my knowledge this is the first report of a non-myeloid/lymphoid cell type making IL-12-p70 in response to an infection. Equally interesting, infected epithelial cells significantly upregulated transforming growth factor alpha precursor expression, suggesting a mechanism by which they might play a direct role in the pathological scarring seen as a consequence of Chlamydia infections. Data from these in vitro studies predict that infected oviduct epithelium contributes significantly to host innate and adaptive defenses but may also participate in the immunopathology seen with Chlamydia infections.

* 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.

Editor: J. D. Clements

Infection and Immunity, July 2004, p. 3951-3960, Vol. 72, No. 7
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.7.3951-3960.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Faherty, C. S., Maurelli, A. T. (2009). Spa15 of Shigella flexneri Is Secreted through the Type III Secretion System and Prevents Staurosporine-Induced Apoptosis. Infect. Immun. 77: 5281-5290 [Abstract] [Full Text]  
  • Jayarapu, K., Kerr, M. S., Katschke, A., Johnson, R. M. (2009). Chlamydia muridarum-Specific CD4 T-Cell Clones Recognize Infected Reproductive Tract Epithelial Cells in an Interferon-Dependent Fashion. Infect. Immun. 77: 4469-4479 [Abstract] [Full Text]  
  • Nagarajan, U. M., Prantner, D., Sikes, J. D., Andrews, C. W. Jr., Goodwin, A. M., Nagarajan, S., Darville, T. (2008). Type I Interferon Signaling Exacerbates Chlamydia muridarum Genital Infection in a Murine Model. Infect. Immun. 76: 4642-4648 [Abstract] [Full Text]  
  • Derbigny, W. A., Hong, S.-C., Kerr, M. S., Temkit, M., Johnson, R. M. (2007). Chlamydia muridarum Infection Elicits a Beta Interferon Response in Murine Oviduct Epithelial Cells Dependent on Interferon Regulatory Factor 3 and TRIF. Infect. Immun. 75: 1280-1290 [Abstract] [Full Text]  
  • Mackern-Oberti, J. P., Maccioni, M., Cuffini, C., Gatti, G., Rivero, V. E. (2006). Susceptibility of Prostate Epithelial Cells to Chlamydia muridarum Infection and Their Role in Innate Immunity by Recruitment of Intracellular Toll-Like Receptors 4 and 2 and MyD88 to the Inclusion. Infect. Immun. 74: 6973-6981 [Abstract] [Full Text]  
  • Roshick, C., Wood, H., Caldwell, H. D., McClarty, G. (2006). Comparison of Gamma Interferon-Mediated Antichlamydial Defense Mechanisms in Human and Mouse Cells. Infect. Immun. 74: 225-238 [Abstract] [Full Text]  
  • Derbigny, W. A., Kerr, M. S., Johnson, R. M. (2005). Pattern Recognition Molecules Activated by Chlamydia muridarum Infection of Cloned Murine Oviduct Epithelial Cell Lines. J. Immunol. 175: 6065-6075 [Abstract] [Full Text]  
  • Nelson, D. E., Virok, D. P., Wood, H., Roshick, C., Johnson, R. M., Whitmire, W. M., Crane, D. D., Steele-Mortimer, O., Kari, L., McClarty, G., Caldwell, H. D. (2005). Chlamydial IFN-{gamma} immune evasion is linked to host infection tropism. Proc. Natl. Acad. Sci. USA 102: 10658-10663 [Abstract] [Full Text]  
  • Nagarajan, U. M., Ojcius, D. M., Stahl, L., Rank, R. G., Darville, T. (2005). Chlamydia trachomatis Induces Expression of IFN-{gamma}-Inducible Protein 10 and IFN-{beta} Independent of TLR2 and TLR4, but Largely Dependent on MyD88. J. Immunol. 175: 450-460 [Abstract] [Full Text]  
  • Virok, D. P., Nelson, D. E., Whitmire, W. M., Crane, D. D., Goheen, M. M., Caldwell, H. D. (2005). Chlamydial Infection Induces Pathobiotype-Specific Protein Tyrosine Phosphorylation in Epithelial Cells. Infect. Immun. 73: 1939-1946 [Abstract] [Full Text]  


Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»