Macrophage produced IL-12p70 mediates hemorrhage-induced damage in a complement dependent manner

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Show simple item record Hylton, Diana J. Hoffman, Sara M. Van Rooijen, N. Tomlinson, Stephen Fleming, Sherry D. 2013-10-16T16:04:17Z 2013-10-16T16:04:17Z 2013-10-16
dc.description.abstract Hemorrhage and hemorrhagic shock instigate intestinal damage and inflammation. Multiple components of the innate immune response, including complement and neutrophil infiltration, are implicated in this pathology. To investigate the interaction of complement activation and other components of the innate immune response during hemorrhage, we treated mice post-hemorrhage with CR2-fH, a targeted inhibitor of the alternative complement pathway and assessed intestinal damage and inflammation 2 h after hemorrhage. In wildtype mice, CR2-fH attenuated hemorrhage-induced, mid-jejunal damage and inflammation as determined by decreased mucosal damage, macrophage infiltration, LTB[subscript 4], IL-12p40, and TNF-α production. The critical nature of intestinal macrophage infiltration and activation in the response to hemorrhage was further determined using mice pre-treated with clodronate containing liposomes. The absence of either macrophages or IL-12p70 attenuated intestinal damage. These data suggest that complement activation and macrophage infiltration with IL-12p70 production are critical to hemorrhage induced mid-jejunal damage and inflammation. en_US
dc.language.iso en_US en_US
dc.relation.uri en_US
dc.rights This is a non-final version of an article published in final form in Shock, 35(2), 134-140. en_US
dc.subject Inflammation en_US
dc.subject Mouse en_US
dc.subject Intestine en_US
dc.subject Cytokines en_US
dc.subject Complement inhibitor en_US
dc.title Macrophage produced IL-12p70 mediates hemorrhage-induced damage in a complement dependent manner en_US
dc.type Article (author version) en_US 2011 en_US
dc.citation.doi doi:10.1097/SHK.0b013e3181ed8ec9 en_US
dc.citation.epage 140 en_US
dc.citation.issue 2 en_US
dc.citation.jtitle Shock en_US
dc.citation.spage 134 en_US
dc.citation.volume 35 en_US
dc.contributor.authoreid sdflemin en_US

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