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Infection and Immunity, April 2007, p. 1690-1697, Vol. 75, No. 4
0019-9567/07/$08.00+0     doi:10.1128/IAI.01564-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Inhibition of Interleukin-22 Attenuates Bacterial Load and Organ Failure during Acute Polymicrobial Sepsis{triangledown}

Georg F. Weber, Sylvia Schlautkötter, Simone Kaiser-Moore, Felicitas Altmayr, Bernhard Holzmann, and Heike Weighardt*

Department of Surgery, Technische Universität München, Ismaninger Strasse 22, 81675 Munich, Germany

Received 28 September 2006/ Returned for modification 11 October 2006/ Accepted 8 January 2007

Interleukin-22 (IL-22) is a recently discovered proinflammatory cytokine, structurally related to IL-10. Since IL-22 is induced by lipopolysaccharide in vivo, we studied the role of IL-22 in a model of polymicrobial peritonitis. Quantitative real-time reverse transcription-PCR analysis showed marked induction of IL-22 and IL-22 receptor in spleen and kidney during the course of sepsis. The biological activity of IL-22 is modulated by IL-22-binding protein (IL-22BP), which is considered a natural antagonist of IL-22. To further analyze the role of IL-22 during septic peritonitis, mice were treated with recombinant IL-22BP generated as Fc{gamma}2a fusion protein. IL-22BP-Fc completely blocked IL-22-induced STAT3 activation in hepatocytes in vitro. Treatment of mice with IL-22BP-Fc 4 h before sepsis induction led to enhanced accumulation of neutrophils and mononuclear phagocytes and a reduced bacterial load at the site of infection. In addition, IL-22 blockade led to an enhanced bacterial clearance in liver and kidney and reduced kidney injury. These results imply an important proinflammatory role of IL-22 during septic peritonitis, contributing to bacterial spread and organ failure. IL-22 therefore appears to play an important role in the regulation of inflammatory processes in vivo.

* Corresponding author. Mailing address: Department of Surgery, Technische Universität München, Ismaninger Strasse 22, 81675 Munich, Germany. Phone: 49-89-4140 6604. Fax: 49-89-4140 6605. E-mail: weighardt{at}chir.med.tu-muenchen.de.

{triangledown} Published ahead of print on 29 January 2007.

Editor: R. P. Morrison

Infection and Immunity, April 2007, p. 1690-1697, Vol. 75, No. 4
0019-9567/07/$08.00+0     doi:10.1128/IAI.01564-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.





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