Neutrophil adherence to isolated adult canine myocytes. Evidence for a CD18-dependent mechanism

M. L. Entman, K. Youker, S. B. Shappell, C. Siegel, R. Rothlein, W. J. Dreyer, F. C. Schmalstieg, C. W. Smith

Research output: Contribution to journalArticle

182 Scopus citations

Abstract

Cardiac myocytes were isolated from adult dogs and incubated with isolated canine neutrophils (PMN). Intercellular adhesion was low and unchanged by stimulation of the PMN with zymosan activated serum or platelet activating factor (PAF) at concentrations that significantly enhance PMN adhesion to protein-coated glass and canine endothelial cell monolayers. Intercellular adhesion was significantly increased only when both myocytes and PMN were stimulated (e.g., myocytes incubated with IL-1, tumor necrosis factor, or phorbol myristate acetate, and PMN were chemotactically stimulated). Inhibitors of protein synthesis diminished the IL-1β-induced effect by > 80%. The IL-1β, PAF-stimulated PMN-myocyte adhesion was associated with substantial H2O2 production. Under conditions with low PMN-myocyte adhesion (i.e., IL-1β alone, PAF alone, or no stimulus) H2O2 production was generally < 5% of that occurring with high adhesion. An anti-CD18 monoclonal antibody (R15.7) inhibited stimulated PMN-myocyte adhesion by > 95% and reduced H2O2 production by > 90%. Control isotype-matched, binding, and nonbinding antibodies were without effect on adherence or H2O2 production. The results indicate that cytokine stimulation of adult myocytes induces expression of a ligand involved in CD18-dependent adherence of canine neutrophils.

Original languageEnglish (US)
Pages (from-to)1497-1506
Number of pages10
JournalJournal of Clinical Investigation
Volume85
Issue number5
DOIs
StatePublished - 1990

Keywords

  • Chemotactic factors
  • Cytokines
  • Endothelium
  • Hydrogen peroxide
  • Monoclonal antibodies

ASJC Scopus subject areas

  • Medicine(all)

Fingerprint Dive into the research topics of 'Neutrophil adherence to isolated adult canine myocytes. Evidence for a CD18-dependent mechanism'. Together they form a unique fingerprint.

Cite this