Diminished Polymorphonuclear Leukocyte Adherence

Abstract

A B S T R A C T To investigate the biochemical and cellular basis for the rise in polymorphonuclear leukocyte (PMN) count during epinephrine administration, PMN from subjects receiving epinephrine were studied for their capacity to adhere to nylon wool fibers and endothelial cell monolayers. After administration of epinephrine, the PMN count increased by 80% at 5 min, and isolated PMN adherence to nylon fibers fell from a base line of44±2-18+3%. In contrast, when subjects were infused with the 13-antagonist propanolol before receiving epinephrine, the PMN count failed to rise and PMN adherence was normal. Exposure of PMN endothelial cell monolayers to 0.1 ,uM epinephrine led to diminished PMN adherence that could be blocked by 10 uM propanolol but not by 10 ,uM phentolamine. Sera obtained from subjects 5 min after receiving epinephrine or from supernates derived from endothelial cell monolayers exposed to 90 nM epinephrine inhibited PMN adherence to nylon fibers. Addition of anticyclic AMP antisera but not anticyclic guanosine monophosphate antisera to the postepinephrine sera or to the postepinephrine supernate derived from the endothelial cell monolayers abolished their inhibitory effect of PMN adherence to nylon fibers. In contrast, direct exposure of PMN to epinephrine failed to affect their adherent properties. Because it has been previously shown that endothelial cells contain 18-receptors and respond to catecholamines by raising their intracellular concentrations ofcyclic AMP, and that PMN adherence is attenuated by cyclic AMP, it would appear that diminished PMN adherence after epinephrine administration is mediated through endothelial cell ,3-receptor activity, which in turn impairs PMN margination in vivo and could account for the rise in circulating PMN.

Synthetic Prostacyclin Analogs Differentially Regulate Macrophage Function via Distinct Analog-Receptor Binding Specificities

“…Regulation of bacterial killing by PGI 2 has only been studied directly in neutrophils, where it was not found to have an effect (25). We find in both AMs and PMs (Fig.…”

“…Little is known about the direct effects of PGI 2 or its analogs on the regulation of leukocyte bactericidal activity (25). We therefore examined the effect of stable PGI 2 analogs on bacterial killing using the Gram-negative pathogen Klebsiella pneumoniae (26).…”

Repetitive hypoglycaemia increases serum adrenaline and induces monocyte adhesion to the endothelium in rat thoracic aorta

“…Although several studies have investigated the role of cAMP in the modulation of adhesion molecule abundance, the findings obtained so far remain controversial. Activation of cAMP has been reported to inhibit the adhesion of polymorphonuclear leucocytes to nylon fibres [27,28]. In contrast, various agents, including adrenaline and noradrenaline, that are known to increase cAMP levels in endothelial cells promote adhesion of monocytes and leucocytes [29][30][31].…”

Degradation of heparan sulfate in the subendothelial extracellular matrix by a readily released heparanase from human neutrophils. Possible role in invasion through basement membranes.

“…On their way from the blood toward an affected tissue the cells must invade across the endothelium of postcapillary venules and the underlying basal lamina (1). This process involves adherence of neutrophils to the endothelial luminal surface, invasion and dissociation of endothelial cell junctions, and active participation of hydrolytic enzymes (2,3). The same is true for virtually every epithelium in the body that is traversed by human neutrophils before they accumulate at the site of inflammation (4).…”