• Matijs van Meurs, Pedro Castro, Nathan I Shapiro, Shulin Lu, Midori Yano, Norikazu Maeda, Tohru Funahashi, Ichiro Shimomura, Jan G Zijlstra, Grietje Molema, Samir M Parikh, William C Aird, and Kiichiro Yano.
• Center for Vascular Biology Research, Beth Israel Deaconess Medical Center/Harvard Medical School, Boston, Massachusetts, USA. m.van.meurs@umcg.nl
• Shock. 2012 Apr 1; 37 (4): 392-8.

AbstractExperimental sepsis was induced in male C57BL/6j, adiponectin-deficient mice (ADPNKO), and wild-type littermates by i.p. injection of 16 mg/kg lipopolysaccharide or cecal ligation and puncture. Blood and tissue samples were harvested 24 h after model induction. Circulating adiponectin is reduced in mice with endotoxemic challenge and after cecal ligation and puncture compared with healthy control mice. Quantitative reverse transcriptase-polymerase chain reaction for adiponectin reveals a pattern of response that is both model- and organ-specific. When challenged with sepsis, adiponectin deficiency results in increased expression of endothelial adhesion and coagulation molecules in the lung, liver, and kidney as quantified by reverse transcriptase-polymerase chain reaction, increased macrophage and neutrophil infiltration by immunohistochemistry, and vascular leakage in the liver and kidney. Adiponectin-deficient mice have reduced survival following cecal ligation and puncture and increased blood levels of interleukin 6, soluble vascular endothelial growth factor receptor 1, and soluble endothelial adhesion molecules E-selectin and intercellular adhesion molecule 1. Finally, ADPNKO promoted end-organ injury in the liver and kidney, whereas the lungs were not affected. These data suggest a protective role of adiponectin in diminishing microvascular organ-specific endothelial cell activation during sepsis.

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