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Infection and Immunity, June 2004, p. 3561-3570, Vol. 72, No. 6
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.6.3561-3570.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Protective Role of Interleukin-6 during Yersinia enterocolitica Infection Is Mediated through the Modulation of Inflammatory Cytokines

Peter H. Dube,1,{dagger} Scott A. Handley,1,{dagger},{ddagger} James Lewis,2,3 and Virginia L. Miller1,4*

Department of Molecular Microbiology,1 Department of Medicine,2 Department of Pathology and Immunology,3 Department of Pediatrics, Washington University School of Medicine, St. Louis, Missouri 631104

Received 4 August 2003/ Returned for modification 30 September 2003/ Accepted 22 February 2004

Yersinia enterocolitica is a gram-negative enteric pathogen responsible for a number of gastrointestinal disorders. A striking feature of the pathology of a Y. enterocolitica infection is inflammation. Recently, we demonstrated a role for interleukin-1{alpha} (IL-1{alpha}) in the establishment of intestinal inflammation in response to a Y. enterocolitica infection. A cytokine directly affected by IL-1 levels is IL-6. A previous report suggested that IL-6 plays an anti-inflammatory role during Y. enterocolitica infection, and in other systems IL-6 has been shown to be proinflammatory. Therefore, a closer examination of the roles of IL-6 and inflammatory cytokines in the control of Y. enterocolitica infection in IL-6–/– mice was undertaken. Y. enterocolitica organisms were more virulent in the IL-6–/– mice (60-fold decreased 50% lethal dose) and colonized systemic tissues more rapidly and to a higher level than in the wild-type mice. One role of IL-6 during a Y. enterocolitica infection may be the downmodulation of the inflammatory response. The IL-6–/– mice have a more robust TH1 T-cell response, as well as hyperinflammatory pathologies. These phenotypes appear to be due to the misregulation of tumor necrosis factor alpha, monocyte chemotactic protein 1, IL-10, transforming growth factor ß1, and gamma interferon in the IL-6–/– mouse. These data provide further insight into the intricate cytokine signaling pathways involved in the regulation of inflammatory responses and the control of bacterial infections.

* Corresponding author. Mailing address: Department of Molecular Microbiology, Washington University School of Medicine, 660 S. Euclid Ave., Campus Box 8230, St. Louis, MO 63110. Phone: (314) 286-2891. Fax: (314) 286-2896. E-mail: virginia{at}borcim.wustl.edu.

Editor: J. T. Barbieri

{dagger} P.H.D. and S.A.H. contributed equally to this study.

{ddagger} Present address: Department of Microbiology and Immunology, University of Texas Health Sciences Center at San Antonio, San Antonio, TX 78229-3900.

Infection and Immunity, June 2004, p. 3561-3570, Vol. 72, No. 6
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.6.3561-3570.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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