Overlapping functions of E- and P-selectin in neutrophil recruitment during acute inflammation

Jonathon W. Homeister, Mengkun Zhang, Paul S. Frenette, Richard O. Hynes, Denisa D. Wagner, John B. Lowe, Rory M. Marks

Research output: Contribution to journalArticle

60 Scopus citations

Abstract

Selectin adhesion molecules mediate leukocyte rolling on activated endothelium, a prerequisite to leukocyte accumulation at sites of inflammation. The precise role of each selectin (E-, P-, and L-) in this process is unclear and may vary depending on the particular inflammatory stimulus, vascular bed, leukocyte subset, and species; most data suggest discrete functional roles for each selectin. To define the relative roles of E- and P-selectin in mediating neutrophil accumulation in acute dermal inflammation, mice genetically deficient in E-selectin, P-selectin, or both E- and P-selectin were injected intradermally with zymosan. Luminal endothelial expression of E- and P-selectin in response to zymosan was documented in wild-type mice by intravenous administration of fluorochrome- labeled anti-E- and anti-Pselectin antibodies. In mice deficient in E- or P- selectin, neutrophil accumulation was unchanged or only subtly reduced relative to wild-type control mice. In mice deficient in both E- and P- selectin, neutrophil accumulation was significantly reduced (87% at 4 hours and 79% at 8 hours). These data demonstrate that, in this model of acute inflammation, there is considerable overlap in the functions of E- and P- selectin; loss of both selectins was required to impair neutrophil accumulation.

Original languageEnglish (US)
Pages (from-to)2345-2352
Number of pages8
JournalBlood
Volume92
Issue number7
StatePublished - Oct 1 1998
Externally publishedYes

ASJC Scopus subject areas

  • Biochemistry
  • Immunology
  • Hematology
  • Cell Biology

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    Homeister, J. W., Zhang, M., Frenette, P. S., Hynes, R. O., Wagner, D. D., Lowe, J. B., & Marks, R. M. (1998). Overlapping functions of E- and P-selectin in neutrophil recruitment during acute inflammation. Blood, 92(7), 2345-2352.