Adherence of neutrophils to canine cardiac myocytes in vitro is dependent on intercellular adhesion molecule-1

C. Wayne Smith, Mark L. Entman, Caryl L. Lane, Arthur L. Beaudet, Theresa I. Ty, Keith Youker, Hal K. Hawkins, D. C. Anderson

Research output: Contribution to journalArticlepeer-review

144 Scopus citations

Abstract

The adhesiveness of isolated canine cardiac myocytes for neutrophils is greatly increased by stimulation with cytokines such as tumor necrosis factor α (TNFα). Since this adhesion is significantly inhibited by an anti-CD 18 MAb, experiments were performed to test the hypothesis that the newly expressed adhesion molecule on the cardiac myocytes was intercellular adhesion molecule-1 (ICAM-1). A newly developed MAb, CL18/6, was found to exhibit the functional and binding characteristics with canine neutrophils and canine jugular vein endothelial cells expected of an antibody recognizing ICAM-1. MAb CL18/6 also bound to isolated cardiac myocytes after stimulation of the myocytes with cytokines, and it blocked by > 90% the adhesion of neutrophils to stimulated myocytes. A partial cDNA clone for canine ICAM-1 was isolated, and ICAM-1 mRN A was found to be increased in both endothelial cells and cardiac myocytes after cytokine stimulation. Cytokines that both increased the CL18/6-inhibitable adhesion of neutrophils to myocytes and induced expression of ICAM-1 were IL-1β, TNFα, and LPS. These results are consistent with the conclusion that canine endothelial cells and cardiac myocytes express ICAM-1 in response to cytokine stimulation, and that ICAM-1 functions as an adhesive molecule for neutrophils on both cell types.

Original languageEnglish (US)
Pages (from-to)1216-1223
Number of pages8
JournalJournal of Clinical Investigation
Volume88
Issue number4
StatePublished - 1991
Externally publishedYes

Keywords

  • Adhesion cytokines
  • ICAM-1
  • Myocyte
  • Neutrophil

ASJC Scopus subject areas

  • General Medicine

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