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Laboratorio di Biologia Cellulare, Fisiopatologia Respiratoria, Dipartimento Cardiotoracico dell'Università di Pisa, 56124 Pisa, Italy
Intercellular
adhesion molecule-1 (ICAM-1) is the only inducible adhesion receptor
for neutrophils identified in bronchial epithelial cells. We stimulated
human airway epithelial cells with various agonists to evaluate whether
ICAM-1-independent adhesion mechanisms could be elicited. Phorbol
12-myristate 13-acetate (PMA) stimulation of cells of the alveolar cell
line A549 caused a rapid, significant increase in neutrophil adhesion
from 11 ± 3 to 49 ± 7% (SE). A significant increase from 17 ± 4 to 39 ± 6% was also observed for neutrophil adhesion to
PMA-stimulated human bronchial epithelial cells in primary culture.
Although ICAM-1 expression was upregulated by PMA at late time points, it was not affected at 10 min when neutrophil adhesion was already clearly enhanced. Antibodies to ICAM-1 had no effect on neutrophil adhesion. In contrast, antibodies to the leukocyte integrin
-chain CD18 totally inhibited the adhesion of neutrophils to PMA-stimulated epithelial cells. These results demonstrate that PMA stimulation of
human airway epithelial cells causes an increase in neutrophil adhesion
that is not dependent on ICAM-1 upregulation.
intercellular adhesion molecule-1; phorbol 12-myristate 13-acetate; lung; inflammation;
2-integrins
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