Consequences of neutrophil adhesion to physiological and pathological targets
Issue title: Proceedings of the Seventh International Congress of Biorheology. Part I. Palais des Congrès, Nancy, France, 18–23 June 1989. Dedicated to Richard Skalak
Guest editors: Alfred L. Copley and Jean-François Stoltz
Affiliations: INSERM U.294, CHU Xavier Bichat, Université Paris 7, France
Note: [] Accepted by: G.W. Schmid-Schönbein
Abstract: The ability of neutrophils to adhere in a coordinated and reversible manner to the endothelium and other tissular components is crucial to their chemoattractant-induced locomotion towards relevant targets. Opsonins play a major role in the killing effect of neutrophils by inducing close adherence between the neutrophil and the target, thus maximizing the effect of the reactive oxygen species released by the stimulated neutrophils. Reactive oxygen species are released together with degradative enzymes and other killing proteins associated with neutrophil degranulation. This targeted neutrophil activity kills invading microorganisms but, in a similar way, may be harmful to organs, cells and molecules that have been altered in some way or are involved in immune reactions. In some other pathological situations where body fluids contain proinflammatory agents, neutrophils may behave in a nontargeted and inappropriate manner. In such cases, adherence is often increased, thus slowing locomotion. Moreover, inflammatory agents often prime neutrophils for the oxidative burst induced by chemoattractants or other stimuli. The combined slow locomotion and hypersensitivity of primed neutrophils leads to a premature release of killing subtances which may affect blood components, vascular cells, connective tissue or whole organs . Any disturbance of neutrophil adherence is thus potentially harmful and must be recognized and suitably treated.
Keywords: Human polymorphonuclear leukocyte, adherence, neutrophil activation, tissue injury
DOI: 10.3233/BIR-1990-273-418
Journal: Biorheology, vol. 27, no. 3-4, pp. 419-424, 1990
