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

Am J Pathol. 2010 Jan;176(1):218-26. doi: 10.2353/ajpath.2010.081027. Epub 2009 Nov 30.

Abstract

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.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Acute Lung Injury / blood
  • Acute Lung Injury / complications*
  • Acute Lung Injury / enzymology
  • Acute Lung Injury / pathology*
  • Alanine Transaminase / blood
  • Animals
  • Aspartate Aminotransferases / blood
  • Biomarkers / metabolism
  • Blood Urea Nitrogen
  • CD11c Antigen / metabolism*
  • Capillaries / drug effects
  • Capillaries / pathology
  • Cytokines / genetics
  • Cytokines / metabolism
  • Diphtheria Toxin / pharmacology
  • Disease Models, Animal
  • Disease Progression
  • Gene Expression Regulation
  • Heparin-binding EGF-like Growth Factor
  • Intercellular Signaling Peptides and Proteins / metabolism
  • Kidney / drug effects
  • Kidney / pathology
  • Lipopolysaccharides
  • Mice
  • Mice, Inbred C57BL
  • Multiple Organ Failure / blood
  • Multiple Organ Failure / complications*
  • Multiple Organ Failure / enzymology
  • Multiple Organ Failure / pathology*
  • Necrosis
  • Oxidative Stress / drug effects
  • Pulmonary Alveoli / blood supply
  • Pulmonary Alveoli / drug effects
  • Pulmonary Alveoli / pathology
  • Solubility / drug effects
  • Survival Analysis

Substances

  • Biomarkers
  • CD11c Antigen
  • Cytokines
  • Diphtheria Toxin
  • Hbegf protein, mouse
  • Heparin-binding EGF-like Growth Factor
  • Intercellular Signaling Peptides and Proteins
  • Lipopolysaccharides
  • Aspartate Aminotransferases
  • Alanine Transaminase