Complement depletion enhances pulmonary inflammatory response after liver injury

Journal of Gastrointestinal Surgery : Official Journal of the Society for Surgery of the Alimentary Tract
Sean C GlasgowWilliam C Chapman

Abstract

Hepatic cryoablation can produce acute lung injury, with activation of nuclear factor (NF)-kappaB in the remnant liver and lungs, production of C-X-C chemokines, and neutrophil infiltration of the lungs. Activated complement stimulates NF-kappaB and cytokine secretion from Kupffer cells. The role of complement in the development of acute lung injury after cryoablation was examined using HLL transgenic mice (5'HIV-LTR-Luciferase gene; 5' HIV-LTR is an NF-kappaB-dependent promoter). Total complement depletion was achieved with preoperative administration of cobra venom factor (CVF). After hepatic cryoablation, bioluminescent NF-kappaB activity increased in the nonablated liver remnant by 4 hours in both control (119,093 +/- 22,808 net RLU/mg protein) and CVF-treated mice (117,722 +/- 14,932) from cumulative baseline (657 +/- 90, P < 0.0001). In the lung, complement-depletion induced significantly greater increases in NF-kappaB activation at both early and later times. Likewise, chemokines were higher in complement-depleted mice relative to controls (KC: 493 +/- 43 versus 269 +/- 29 pg/mg protein, P < 0.001; MIP-2: 171 +/- 29 versus 64 +/- 13 pg/mg protein, P < 0.0001). Pulmonary myeloperoxidase activity was equivalent at 24 hours...Continue Reading

Citations

Jun 5, 2007·American Journal of Physiology. Lung Cellular and Molecular Physiology·Sean C GlasgowWilliam C Chapman

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