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Infection and Immunity, December 2007, p. 5924-5929, Vol. 75, No. 12
0019-9567/07/$08.00+0     doi:10.1128/IAI.01029-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

The Extracellular Signal-Regulated Kinase/Mitogen-Activated Protein Kinase Pathway Induces the Inflammatory Factor Interleukin-8 following Chlamydia trachomatis Infection{triangledown}

Kerry R. Buchholz1 and Richard S. Stephens1,2*

Program in Infectious Diseases and Immunity,1 the School of Public Health, University of California, Berkeley, 140 Warren Hall, Berkeley, California 947202

Received 26 July 2007/ Returned for modification 5 September 2007/ Accepted 11 September 2007

Diseases associated with Chlamydia infection, such as pelvic inflammatory disease and ectopic pregnancy, are due to inflammation-mediated tissue damage and scarring that occur after chronic or repeated infections. The inflammatory chemokine interleukin-8 (IL-8) is produced by Chlamydia-infected cells through an endogenous mechanism of activation, independent of soluble factors in the supernatant. The host signaling pathways necessary for this response are not understood, but the mitogen-activated protein kinase (MAPK) extracellular signal-regulated kinase (ERK) has been shown to be activated at similar times as IL-8 mRNA up-regulation. The purpose of this study was to elucidate the MAPK pathways necessary to induce the endogenous IL-8 response to Chlamydia trachomatis infection of epithelial cells. IL-8 induced by infection with C. trachomatis L2 was shown to be dependent on ERK and independent of p38 and Jun N-terminal MAPK by use of chemical inhibitors of the signaling pathways. Persistent ERK activation during IL-8 mRNA production at 24 h postinfection was necessary to maintain the response. C. trachomatis serovar D also induced IL-8 in an ERK-dependent manner. We concluded that IL-8 induced during infection of epithelial cells is dependent on continual activation of ERK by C. trachomatis.

* Corresponding author. Mailing address: Division of Infectious Diseases, School of Public Health, 140 Warren Hall, University of California—Berkeley, Berkeley, CA 94720. Phone: (510) 643-9900. Fax: (510) 643-1537. E-mail: rss{at}berkeley.edu

{triangledown} Published ahead of print on 24 September 2007.

Editor: A. J. Bäumler

Infection and Immunity, December 2007, p. 5924-5929, Vol. 75, No. 12
0019-9567/07/$08.00+0     doi:10.1128/IAI.01029-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • de la Torre, E., Mulla, M. J., Yu, A. G., Lee, S.-J., Kavathas, P. B., Abrahams, V. M. (2009). Chlamydia trachomatis Infection Modulates Trophoblast Cytokine/Chemokine Production. J. Immunol. 182: 3735-3745 [Abstract] [Full Text]  
  • Voth, D. E., Heinzen, R. A. (2009). Sustained Activation of Akt and Erk1/2 Is Required for Coxiella burnetii Antiapoptotic Activity. Infect. Immun. 77: 205-213 [Abstract] [Full Text]  
  • Buchholz, K. R., Stephens, R. S. (2008). The Cytosolic Pattern Recognition Receptor NOD1 Induces Inflammatory Interleukin-8 during Chlamydia trachomatis Infection. Infect. Immun. 76: 3150-3155 [Abstract] [Full Text]  


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