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The Journal of Immunology, 1999, 162: 423-434.
Copyright © 1999 by The American Association of Immunologists

Triggering of Chloride Ion Efflux from Human Neutrophils as a Novel Function of Leukocyte ß2 Integrins: Relationship with Spreading and Activation of the Respiratory Burst1

Renzo Menegazzi2, Sara Busetto, Eva Decleva, Rita Cramer, Pietro Dri and Pierluigi Patriarca

Department of Physiology and Pathology, University of Trieste, Trieste, Italy

PMN residing on immobilized fibronectin have been shown to respond to TNF with an intense and long lasting Cl- efflux that leads to a marked decrease of the unusually high basal Cl- content of these phagocytes. The finding that this Cl- efflux depends, at least in part, on ß2 integrin engagement stimulated the present investigation, which addresses the question as to whether ß2 integrins per se, in the absence of PMN agonists, are able to generate signals triggering Cl- efflux. We induced ß2 integrin cross-linking by plating PMN onto surface-bound mAbs directed against either the common ß-chain (CD18) or the individual {alpha}-chains (CD11a, CD11b, CD11c) of LFA-1, CR3, and gp150/95. Anti-CD18 mAbs triggered a marked release of Cl- ions, which was accompanied by spreading and activation of the respiratory burst. Cross-linking of gp150/95 and LFA-1 generated the most powerful signals for the activation of Cl- efflux. The results of three independent experimental approaches, i.e., kinetic studies, use of Cl- transport inhibitors, and modulation of Cl- efflux with different amounts of anti-ß2 integrin mAbs, indicated that Cl- efflux regulates both spreading and respiratory burst triggered by ß2 integrin cross-linking. Cl- efflux appears to be independent on either alterations of [Ca2+]i or changes in the plasma membrane potential and shows sensitivity to a raise in pHi. This study uncovers a new signaling ability of ß2 integrins and contributes to highlight the role of Cl- efflux in the outside-in signal transduction pathway regulating adherence-dependent PMN responses.




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