ICAM-1-independent adhesion of neutrophils to phorbol ester-stimulated human airway epithelial cells

A Celi, S Cianchetti, S Petruzzelli… - … of Physiology-Lung …, 1999 - journals.physiology.org
A Celi, S Cianchetti, S Petruzzelli, S Carnevali, F Baliva, C Giuntini
American Journal of Physiology-Lung Cellular and Molecular …, 1999journals.physiology.org
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 …
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 β-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.
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