title: Upregulation of ICAM-1 on cardiomyocytes in jeopardized human myocardium during infarction.
abstract: OBJECTIVE
  Impaired perfusion of the myocardium induces a local inflammatory response. In animal models, there is ample evidence that polymorphonuclear leucocytes (PMNs) infiltrating infarcted myocardium contribute significantly to infarct size.
  
  
  METHODS
  To explore a possible role for PMNs in the tissue damage of human myocardial infarction, we investigated localization of intercellular adhesion molecule-1 (ICAM-1) and CD66b (previously clustered as CD67), a marker of degranulation of human PMNs, in relation to deposition of complement in tissue specimens of infarcted and healthy parts of the heart obtained from 20 patients, who had died following acute myocardial infarction.
  
  
  RESULTS
  ICAM-1 was transiently expressed by endothelium and for a longer period (few days) on myofibers of infarcted myocardium. This expression only occurred in parts that stained positive for complement. PMN infiltration exclusively occurred in areas with ICAM-1 expression, but not every ICAM-1-positive area contained PMN infiltrates. CD66b was found in PMNs but was also fixed to the plasma membrane of myofibers that stained positive for complement and ICAM-1.
  
  
  CONCLUSIONS
  These findings indicate that, in infarcted human myocardium, PMNs are degranulated, possibly upon interaction with ICAM-1 and activated complement.
authors.affiliation: Department of Pathology, Free University Hospital, Amsterdam, The Netherlands. pathol@azvu.nl
authors.forename: H W
authors.initials: HW
authors.lastname: Niessen
authors.forename: W K
authors.initials: WK
authors.lastname: Lagrand
authors.forename: C A
authors.initials: CA
authors.lastname: Visser
authors.forename: C J
authors.initials: CJ
authors.lastname: Meijer
authors.forename: C E
authors.initials: CE
authors.lastname: Hack
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D015703:Antigens, CD; D000951:Antigens, Neoplasm; D015815:Cell Adhesion Molecules; D015550:Cell Degranulation; D003167:Complement Activation; D003181:Complement C4 / Q000032:analysis; D015935:Complement C4b; D005260:Female; D058851:GPI-Linked Proteins; D006801:Humans; D007150:Immunohistochemistry; D018799:Intercellular Adhesion Molecule-1 / Q000032:analysis / Q000378:metabolism*; D008297:Male; D008562:Membrane Glycoproteins / Q000032:analysis; D008875:Middle Aged; D009203:Myocardial Infarction / Q000276:immunology*; D009206:Myocardium / Q000276:immunology*; D009504:Neutrophils / Q000378:metabolism / Q000502:physiology; D010446:Peptide Fragments / Q000032:analysis
chemical_list: D015703:Antigens, CD; D000951:Antigens, Neoplasm; C504120:CEACAM8 protein, human; D015815:Cell Adhesion Molecules; D003181:Complement C4; D058851:GPI-Linked Proteins; D008562:Membrane Glycoproteins; D010446:Peptide Fragments; D018799:Intercellular Adhesion Molecule-1; D015935:Complement C4b; C032261:complement C4d