Kupffer cell depletion reduces hepatic inflammation and apoptosis but decreases survival in abdominal sepsis

• DOI: 10.1097/meg.0b013e32833847db
• Publication Date: 2010-03-18T09:34:32Z
• Authors: Tobias Traeger; Marlene Mikulcak; Christian Eipel; Kerstin Abshagen; Stephan Diedrich; Claus-Dieter Heid...; Stefan Maier; Brigitte Vollmar
• Keywords: Kupffer cell

Objective During abdominal sepsis, the activation of hepatic Kupffer cells (KC) and its consequences are central interest. This study evaluates impact selective KC depletion on microcirculation, cytokine release, systemic alterations in colon ascendens stent peritonitis (CASP), a model polymicrobial sepsis. Methods For clodronate liposomes were injected 24 h before CASP surgery female C57BL/6N mice. Three 12 after CASP, in-vivo fluorescence microscopy liver was performed. Analysis hepatocellular apoptosis conducted by immunohistochemistry. In addition, levels tumor necrosis factor (TNF), IL-6, IL-10 liver, lungs, spleen, plasma determined, bacteriology survival analysis Results led to significant sinusoidal perfusion failure, increased leukocyte recruitment, TNF, plasma. significantly reduced recruitment apoptosis. secretion decreased dramatically KC-depleted septic contrast, TNF clearly elevated treatment. lung compensatory upregulation could be detected depletion. Clodronate treatment resulted reduction survival. Conclusion The results indicate that is locally protective as it reduces inflammation These effects observed presence levels. However, lack mice detrimental proinflammation.