Neutrophil migration across monolayers of cytokine-prestimulated endothelial cells: a role for platelet-activating factor and IL-8.

Abstract

Abstract. In a previous study we observed that neutrophils respond with a rapid rise in [Ca2+]; during adherence to cytokine-activated endothelial cells (EC), caused by EC membrane-associated platelet-activating factor (PAF) . In the present study, we investigated whether this form of PAF was important in neutrophil adherence and migration across monolayers of rIL-lß-or ITNFa-prestimulated EC. PAF receptor antagonists prevented neutrophil migration across cytokine-pretreated EC by -60% (P < 0.005) without interfering with the process of adherence . The antagonists WEB 2086 and L-652,731 had no effect on neutrophil migration across resting EC induced by formylmethionyl-leucyl-phenylalanine (FMLP) . A murine T RANSMIGRATION of neutrophils from the peripheral circulation into inflammatory sites requires neutrophil adherence to the endothelial cell lining of the blood vessels. The CD18 complex proteins are: lymphocyte function-associated antigen-1 (LFA-1),' complement receptor 3 (CR3) or Mac-1, and glycoprotein 150,95 (p150,95) . On neutrophils they are involved in both migration and adherence (Anderson et al ., 1985 ;Harlan, 1985 ;Kuijpers and Roos, 1989). In these processes, endothelial intercellular adhesion molecule-1 (ICAM-1) may function as a cellular ligand for LFA-1 and CR3 (Rotplein et al., 1986 ;Diamond et al ., 1990;Springer, 1990) . Its expression can be increased by the inflammatory cytokines interleukin-1 (IL-1) and tumor necrosis factor (TNF) Springer, 1990) .Several other adhesion molecules can play an accessory role in the process of neutrophil adherence . The role of a 1. Abbreviations used in this paper: CR3, complement receptor 3 ; EC, endothelial cells ; ELAM-1, endothelial leukocyte adhesion molecule-l ; FMLP, formyl-leucyl-methionyl-phenylalanine ; HSA, human serum albumin ; ICAM-1, intercellular adhesion molecule-1 ; IL-1, interleukin-1 ; LAM-1, leukocyte adhesion molecule-1 ; LFA-1, lymphocyte-function associated antigen-1; MFI, mean fluorescence intensity ; PAF, platelet-activating factor, p150,95, (glyco)protein 150,95 ; rIL-1p, recombinant interleukin-lß ; rIL-8, recombinant interleukin-8 ; rTNFct, recombinant tumor necrosis fkctor-a ; TNF, tumor necrosis factor.

Involvement of hepatocyte growth factor in increased integrin expression on HepG2 cells triggered by adhesion to endothelial cells

“…LFA-1, the ligand for ICAM-1, and VLA-4, the ligand for VCAM-1, are abundantly expressed on leucocytes. In contrast to this, expression of LFA-1 or VLA-4 is relatively rare in epithelial cancer cells, while a2, a3, a6, Bi and 4 integrin subunits are commonly expressed on most cancer cells (Weinel et al, 1992;Albelda, 1993;Volpes et al, 1993;our (Kuijpers et al, 1992;Tanaka et al, 1993). In the case of HepG2 cells, MIP-1, and IL-8 were devoid of any detectable effect on integrin expression.…”

Protease activation of calcium-independent phospholipase A2 leads to neutrophil recruitment to coronary artery endothelial cells

“…Prescott et al [37] have correlated the adhesion of neutrophils to thrombin-activated endothelium with PAF synthesis and expression on the surface of endothelial cells. Additionally, Kuijpers et al [38] were able to demonstrate the ability of PAF receptor antagonists to prevent neutrophil migration across cytokine pretreated endothelial cells by approximately 60 percent. As our data indicates, the increase in PAF production (Fig.…”

The pathogenesis of transfusion‐related acute lung injury (TRALI)

“…Additional stimuli come from endothelial cells as well, because, once activated, they produce a broad range of chemokines/cytokines, including PAF, leukotriene B4, and IL-8. These substances are not only secreted, but remain also bound to the endothelial cell surface, where they have access to their corresponding receptors on the surface of sequestered and/or adherent neutrophils (Kuijpers et al, 1992). Various substances have been identified as endothelial cell activators, including TNF-a, IL-1b, and other mediators released during inflammatory processes, as well as exogenous LPS and antibodies.…”