The effects of platelet activating factor and retinoic acid on the expression of ELAM-1 and ICAM-1 and the functions of neutrophils

Si-Feng Chen

doi:10.1155/s0962935195000172

Abstract

Preincubation of pulmonary microvascular endothelial cells (PMVECs) with platelet-activating factor (PAF) for 3.5 h increased the adhesion rate of polymorphonuclear leukocytes (PMNs) to PMVECs from 57.3% to 72.8% (p < 0.01). Preincubation of PMNs with PAF also increased PMN-PMVEC adhesion rate. All-trans retinoic acid (RA) blocked the adherence of untreated PMNs to PAF-pretreated PMVECs but not the adherence of PAF-pretreated PMNs to untreated PMVECs. PAF increased the expression of intercellular adhesion molecule-1 (ICAM-1) and E-selection (ELAM-1) on PMVECs, PMN chemotaxis to zymosan-activated serum and histamine, and PMN aggregation and the release of acid phosphatase from PMNs. Co-incubation of RA inhibited PAF-induced PMN aggregation, the release of acid phosphatase from PMNs, and PMN chemotaxis to zymosan-activated serum and histamine while the expression of ICAM-1 and ELAM-1 did not change. Our results suggest that RA can be used to ameliorate PMN-mediated inflammation.

Highlights

Polymorphonuclear neutrophils (PMNs) play a key role in the inflammatory response underlying many diseases
All-trans retinoic acid, Dulbecco’s Modified Eagle Medium (DMEM) and dextran T500 were purchased from Sigma
retinoic acid (RA) did not block the adhesion of PAF-pretreated PMNs to pulmonary microvascular endothelial cells (PMVECs) (Fig.. 1)

Summary

Introduction

Polymorphonuclear neutrophils (PMNs) play a key role in the inflammatory response underlying many diseases. PMNs are capable of chemotaxis, phagocytosis, oxygen-free radical production, and degranulation in response to a variety of stimuli. Overstimulation of PMNs can result in host tissue injury. Inhibition of PMN functions may be beneficial to inflammatory diseases such as systemic inflammatory reaction syndrome. Leukocytes may adhere firmly in microvascular endothelial cells (ECs) whereupon they project pseudopodia and migrate across endothelial monolayers into traumatized interstitia through diapedesis. The localized adhesion of leukocytes to ECs is mediated at least partly by adhesion molecules on leukocytes and their counterpart molecules on ECs such as intercellular adhesion molecule-1 (ICAM1) and E-selectin (ELAM-1)

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Results

Conclusion