Intratracheal administration of endotoxin and cytokines: VIII. LPS induces E-selectin expression; anti-E-selectin and soluble E-selectin inhibit acute inflammation

Thomas R. Ulich, Susan C. Howard, Daniel G. Remick, Eunhee S. Yi, Tucker Collins, Kaizhi Guo, Songmei Yin, Jeffery L. Keene, Jon J. Schmuke, Christina N. Steininger, Joseph K. Welply, James H. Williams

Research output: Contribution to journalArticlepeer-review

43 Scopus citations

Abstract

E-selectin is an inducible endothelial adhesion molecule that binds neutrophils. E-selectin mRNA is not constitutively detectable in the lungs of rats. Intratracheal injection of LPS induces pulmonary E-selectin mRNA expression at 2-4 h. Intratracheal injection of LPS followed at 2 and 4 h by intravenous injection of mouse F(ab′)2 or F(ab′)) anti-E-selectin monoclonal antibody inhibits the emigration of neutrophils into the bronchoalveolar space at 6 h by 50-70%. TNF and IL-6 bioactivity are not decreased in bronchoalveolar lavage fluid after treatment with anti-E-selectin antibody as compared to controls, suggesting that the anti-E-selectin does not affect the magnitude of the LPS-initiated cytokine cascade. Intratracheal injection of LPS followed at 2 and 4 h by intravenous injection of soluble E-selectin inhibits neutrophilic emigration at 6 h by 64%, suggesting that endogenous soluble E-selectin shed from activated endothelium may play a role in the endogenous down-regulation of acute inflammation. E-selectin-mediated adhesion of neutrophils to endothelium appears crucial to the full development of the acute inflammation response.

Original languageEnglish (US)
Pages (from-to)389-398
Number of pages10
JournalInflammation
Volume18
Issue number4
DOIs
StatePublished - Aug 1994

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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