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Am J Physiol Lung Cell Mol Physiol 277: L465-L471, 1999;
1040-0605/99 $5.00
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Vol. 277, Issue 3, L465-L471, September 1999

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

Alessandro Celi, Silvana Cianchetti, Stefano Petruzzelli, Stefano Carnevali, Filomena Baliva, and Carlo Giuntini

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 beta -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; beta 2-integrins


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