• Cytokine · Jan 2009

    IL-10 deficiency augments acute lung but not liver injury in hemorrhagic shock.

    • Philipp Kobbe, Burkhard Stoffels, Joachim Schmidt, Takeshi Tsukamoto, Dmitry W Gutkin, Anthony J Bauer, and Hans-Christoph Pape.
    • Department of Orthopaedic Surgery, University of Pittsburgh, Kaufmann Medical Building, Suite 1010, 3471 Fifth Avenue, Pittsburgh, PA 15213, USA. Kobbe.Philipp@gmx.de
    • Cytokine. 2009 Jan 1; 45 (1): 26-31.

    AbstractIn hemorrhagic shock and trauma, patients are prone to develop systemic inflammation with remote organ dysfunction, which is thought to be caused by pro-inflammatory mediators. This study investigates the role of the immuno-modulatory cytokine IL-10 in the development of organ dysfunction following hemorrhagic shock. Male C57/BL6 and IL-10 KO mice were subjected to volume controlled hemorrhagic shock for 3h followed by resuscitation. Animals were either sacrificed 3 or 24h after resuscitation. To assess systemic inflammation, serum IL-6, IL-10, KC, and MCP-1 concentrations were measured with the Luminex multiplexing platform; acute lung injury (ALI) was assessed by pulmonary myeloperoxidase (MPO) activity and lung histology and acute liver injury was assessed by hepatic MPO activity, hepatic IL-6 levels, and serum ALT levels. There was a trend towards increased IL-6 and KC serum levels 3h after resuscitation in IL-10 KO as compared to C57/BL6 mice; however this did not reach statistical significance. Serum MCP-1 levels were significantly increased in IL-10 KO mice 3 and 24 h following resuscitation as compared to C57/BL6 mice. In IL-10 KO mice, pulmonary MPO activity was significantly increased 3 h following resuscitation and after 24 h histological signs of acute lung injury were more apparent than in C57/BL6 mice. In contrast, no significant differences in any liver parameters were detected between IL-10 KO and C57/BL6 mice. Our data indicate that an endogenous IL-10 deficiency augments acute lung but not liver injury following hemorrhagic shock.

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