Cytokines are causally involved in the natural course of inflammation during sepsis. IL-22 is a recently discovered pro-inflammatory cytokine. The biological activity of IL-22 is considered to be modulated by IL-22-binding protein (BP), which is regarded as a natural antagonist of IL-22. We studied the role of IL-22 in a model of polymicrobial peritonitis. RT-PCR analysis showed an induction of IL-22 and IL-22 receptor in both liver and spleen during the course of sepsis. To further analyse the role of IL-22 during septic peritonitis we pre-treated mice with recombinant IL-22-BP to block IL-22 action. IL-22-BP was generated as Fc-gamma2a-fusion-protein to prolong the half-life time in vivo. Pre-treatment of mice with IL-22-BP/Fc-gamma2a 4h before sepsis induction lead to enhanced accumulation of neutrophils and monocytes/macrophages and a reduced bacterial load in the peritoneal cavity. In addition, IL-22 blockade caused an enhanced bacterial clearance in liver and kidney and reduced kidney injury 12h after sepsis induction. These results imply an important role of IL-22 during septic peritonitis, contributing to bacterial spread and organ failure.
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Cytokines are causally involved in the natural course of inflammation during sepsis. IL-22 is a recently discovered pro-inflammatory cytokine. The biological activity of IL-22 is considered to be modulated by IL-22-binding protein (BP), which is regarded as a natural antagonist of IL-22. We studied the role of IL-22 in a model of polymicrobial peritonitis. RT-PCR analysis showed an induction of IL-22 and IL-22 receptor in both liver and spleen during the course of sepsis. To further analyse the...
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