Endotoxin protection from oxygen toxicity: Effect on pulmonary neutrophils and L-selectin

Susan E. Keeney, Mary J. Mathews, Karen E. Shattuck, Dara V. Dallas

Research output: Contribution to journalArticle

3 Scopus citations

Abstract

The mechanisms by which sublethal doses of endotoxin protect against hyperoxic lung injury are not completely understood. We hypothesized that endotoxin treatment would result in a decreased inflammatory response to hyperoxia and that this would be accompanied by activation of neutrophils (as evidenced by loss of L-selectin) in the peripheral circulation. Adult rats were injected with endotoxin 0.5 mg/kg prior to and 24 hr after onset of exposure to ≥98% O2. After 56 hr of hyperoxia, pulmonary neutrophils were lower in the O2/endotoxin group compared to O2 controls as measured by myeloperoxidase in lung homogenates and neutrophil counts in bronchoalveolar lavage fluid. Circulating neutrophils were also significantly lower in the O2/endotoxin group compared to O2 controls at 56 hr. Expression of the neutrophil adhesion molecule, L-selectin, was lower at 4 and 24 hr in the endotoxin-treated rats compared to O2 controls. There were no differences at 48 hr. Expression of CD18 rose significantly in the O2/endotoxin group after 4 hr, but thereafter did not differ from O2 controls. In summary, endotoxin protection from O2 toxicity was associated with reduced neutrophils in the lung and a loss of L-selectin from peripheral blood neutrophils.

Original languageEnglish (US)
Pages (from-to)243-252
Number of pages10
JournalInflammation
Volume26
Issue number5
DOIs
StatePublished - Oct 1 2002

    Fingerprint

Keywords

  • Adhesion molecules
  • L-selectin
  • Lipopolysaccharide
  • Lung
  • Selectins

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

Cite this