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  • CD11c+ cells are required to prevent progression from local acute lung injury to multiple organ failure and death.

CD11c+ cells are required to prevent progression from local acute lung injury to multiple organ failure and death.

The American journal of pathology (2009-12-02)
Jami E Milam, John R Erb-Downward, Gwo-Hsiao Chen, Marcin F Osuchowski, Roderick McDonald, Stephen W Chensue, Galen B Toews, Gary B Huffnagle, Michal A Olszewski
摘要

To investigate the role of CD11c(+) cells in endotoxin-induced acute lung injury, wild-type or CD11c-diphtheria toxin receptor transgenic mice were treated with intraperitoneal diphtheria toxin (5 ng/g b.wt.) in the presence or absence of intratracheal lipopolysaccharide (51 microg). Lipopolysaccharide treatment resulted in 100% mortality in CD11c-depleted animals but not in control animals. Analysis of local lung tissue revealed no differences in acute lung injury severity; however, analysis of distal tissues revealed severe damage and necrosis to multiple organs (liver, spleen, and kidneys) in CD11c-diphtheria toxin receptor mice but not in wild-type mice. In addition, dramatic increases in systemic levels of liver enzymes (alanine aminotransferase, 657 U/L, aspartate aminotransferase, 1401 U/L), blood urea (53 mg/dl), and 8-iso-prostaglandin F(2alpha), a marker of oxidative stress (350 pg/ml), were observed. These data demonstrate that CD11c(+) cells play a critical role in protecting the organs from systemic injury caused by a pulmonary endotoxin challenge.

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Sigma-Aldrich
E-TOXATE 试剂盒, sufficient for 20 assays