| First Author | Milam JE | Year | 2010 |
| Journal | Am J Pathol | Volume | 176 |
| Issue | 1 | Pages | 218-26 |
| PubMed ID | 19948830 | Mgi Jnum | J:156379 |
| Mgi Id | MGI:4420480 | Doi | 10.2353/ajpath.2010.081027 |
| Citation | Milam JE, et al. (2010) CD11c+ cells are required to prevent progression from local acute lung injury to multiple organ failure and death. Am J Pathol 176(1):218-26 |
| abstractText | 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. |
