Evidence for the involvement of phosphatidylinositol 3-kinase in fMLP-stimulated neutrophil adhesion to ICAM-1-transfected cells

Fabio Pellegatta, Antonella Radaelli, Silvia Heltai, Lu Yan, Sergio L. Chierchia, Franco Folli

Research output: Contribution to journalArticlepeer-review

11 Scopus citations

Abstract

Phosphatidylinositol 3-kinase (PI-3K) controls important intracellular steps involved in inflammation, immunity, and cell growth. PI-3K also modulates leukocyte integrin adhesiveness. In this study we evaluated the role of PI-3K on neutrophil adhesion to intercellular adhesion molecule-1 (ICAM-1)-transfected cells. N-formyl-methionyl-leucyl-phenylalanine (fMLP)-stimulated neutrophil adhesion was inhibited by wortmannin and LY294002, two unrelated PI-3K inhibitors, whereas phorbol myristate acetate (PMA)-induced neutrophil adhesion was not inhibited by them. After fMLP stimulation, a rapid activation of AKT and ERK was observed. However, only activation of AKT was reversed by the PI-3K inhibitors. Neutrophil expression of the β2-integrins Mac-1, lymphocyte function -associated antigen-1(LFA-1.), and gp150.95 was not affected by wortmannin, nor was expression of the activation epitope recognized by MAB24. We conclude that (a) PI-3K is involved in fMLP-activated neutrophil adhesion to ICAM- 1-transfected cells, (b) the mechanism involved is not mediated by the modulation of β2-integrin expression or activation, and (c) another mechanism seems to involve the adhesion to ICAM-1 when a cellular system of adhesion is used.

Original languageEnglish (US)
Pages (from-to)751-761
Number of pages11
JournalJournal of Cardiovascular Pharmacology
Volume37
Issue number6
DOIs
StatePublished - Jun 7 2001

Keywords

  • Intercellular adhesion molecule-1
  • Phosphatidylinositol 3-kinase
  • β-Integrins-Neutrophils

ASJC Scopus subject areas

  • Pharmacology
  • Cardiology and Cardiovascular Medicine

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