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. CONCLUSION: These findings indicate that, in infarcted human myocardium, PMNs are degranulated, possibly upon interaction with ICAM-1 and activated complement
Original language | English |
---|---|
Pages (from-to) | 603-610 |
Number of pages | 8 |
Journal | Cardiovascular research |
Volume | 41 |
Issue number | 3 |
DOIs | |
Publication status | Published - Mar 1999 |
Keywords
- Aged
- Aged, 80 and over
- Antigens, CD
- Antigens, Neoplasm
- Cell Adhesion Molecules
- Cell Degranulation
- Complement Activation
- Complement C4
- Complement C4b
- Female
- GPI-Linked Proteins
- Humans
- Immunohistochemistry
- Intercellular Adhesion Molecule-1
- Journal Article
- Male
- Membrane Glycoproteins
- Middle Aged
- Myocardial Infarction
- Myocardium
- Neutrophils
- Peptide Fragments
- Research Support, Non-U.S. Gov't