Antiadhesive properties of biological surfaces are protective against stimulated granulocytes.
Open Access
- 1 August 1985
- journal article
- research article
- Published by American Society for Clinical Investigation in JCI Insight
- Vol. 76 (2), 535-542
- https://doi.org/10.1172/jci112003
Abstract
Despite the fact that a series of endogenous and exogenous inflammatory mediators are potent activators of circulating granulocytes, damage of vascular endothelium, a primary target tissue, is a rather unusual event in systemic inflammatory states. Since mediator-induced neutrophil hyperadhesiveness on plastic tissue culture dishes is invariably accompanied by intense release of lysosomal granule constituents and respiratory burst activation, thus representing a powerful model to investigate neutrophil cytotoxic states, comparative studies with neutrophils suspended in autologous plasma in the presence or absence of N-formyl-Met-Leu-Phe (2.5 microM), the most potent adhesion inducer, were performed on different biologic surfaces. On optimally adherent closed monolayers of cultured endothelial cells or fibroblasts we observed poor stimulation of adhesion as well as minimal granule release and hexose monophosphate pathway activation. Functional behavior of neutrophils on single molecular components of basal laminas such as fibronectin and collagen (type IV) coats was intermediate, with positive adhesion promotion but markedly reduced metabolic activation. When tested on endothelial cell-derived extracellular matrices, neutrophils again showed functional nonresponsiveness to N-formyl-Met-Leu-Phe. Scanning electron microscopy revealed an impressive congruency between the degree of cellular spreading and metabolic activation in the presence of N-formyl-Met-Leu-Phe, with maximally flattened neutrophils on plastic vs. nonspread, polarized cells on monolayers. Identical results were obtained by using other adhesion inducers such as complement-activated plasma or endotoxin. Lack of cell injury by N-formyl-Met-Leu-Phe-exposed neutrophils was corroborated by the absence of tracer release from [111In]tropolonate-labeled endothelium. These results indicate that biologic surfaces possess antiadhesive properties that protect them from cytotoxic damage by stimulated angry phagocytes.This publication has 30 references indexed in Scilit:
- Proton secretion by stimulated neutrophils. Significance of hexose monophosphate shunt activity as source of electrons and protons for the respiratory burst.JCI Insight, 1984
- Glutathione redox cycle protects cultured endothelial cells against lysis by extracellularly generated hydrogen peroxide.JCI Insight, 1984
- The respiratory burst of phagocytes.JCI Insight, 1984
- Adult Respiratory-Distress SyndromeNew England Journal of Medicine, 1982
- The labelling of blood cells in plasma with111In-tropolonateThe British Journal of Radiology, 1982
- Receptor-directed inhibition of chemotactic factor-induced neutrophil hyperactivity by pyrazolon derivatives. Definition of a chemotactic peptide antagonist.JCI Insight, 1980
- Release of Inflammatory Mediators from Stimulated NeutrophilsNew England Journal of Medicine, 1980
- Virus Infection of Endothelial Cells Increases Granulocyte AdherenceJCI Insight, 1980
- Modulating Influence of Chemotactic Factor-Induced Cell Adhesiveness on Granulocyte FunctionJCI Insight, 1979
- Oxygen radicals mediate endothelial cell damage by complement-stimulated granulocytes. An in vitro model of immune vascular damage.JCI Insight, 1978