Interleukin 1 acts on cultured human vascular endothelium to increase the adhesion of polymorphonuclear leukocytes, monocytes, and related leukocyte cell lines.

Abstract

Increased leukocyte adhesion to the endothelial lining of blood vessels is an essential event in inflammation and the pathogenesis of certain vascular diseases. We have studied the effect of interleukin 1 (IL-1), an inflammatory/immune mediator, on endothelial-leukocyte adhesion using quantitative in vitro assays. Selective pretreatment of cultured human umbilical vein endothelial monolayers with IL-1 (5 U/ml, 4 h) resulted in an 18.3±2.6-fold increase in human peripheral blood polymorphonuclear leukocyte (PMN) adhesion (mean±SEM, n = 16) and a 2.6±0.3-fold increase in monocyte adhesion (n = 7) over basal levels. IL-i-treated endothelial monolayers also supported increased adhesion of the promyelocytic cell line HL-60 and the monocytelike cell line U937 (33.0±6.0-fold, n = 6 and 4.9±0.5-fold, n = 15, respectively). In contrast, selective IL-1 pretreatment of leukocytes, or the addition of IL-1 during the adhesion assay, did not alter endothelial-leukocyte adhesion. Conditioned medium from IL-i-treated endothelial cultures also did not promote leukocyte adhesion to untreated monolayers. IL-i induction of endothelial adhesivity was concentration dependent (maximum, 10 U/ml), time dependent (peak, 4-6 h), and reversible, was blocked by cycloheximide (10 gg/ml) or actinomycin D (5 ,gg/ml) but not by acetylsalicylic acid (100 .M), and occurred without detectable endothelial cell damage. IL-1 treatment of SV40-transformed human endothelial cells and dermal fibroblasts did not increase their adhesivity for leukocytes. These data suggest that IL-1 can act selectively on human vascular endothelium to increase its adhesivity for circulating blood leukocytes, and thus to localize leukocyte-vessel wall interactions at sites of inflammation in vivo.

The effect of herpesvirus infection on the expression of cell adhesion molecules on cultured human dermal microvascular endothelial cells

“…However, the expression of E-selectin was rapid: it had a transient peak at 1 h after treatment with HSV-1 and disappeared within 24 h. This result indicated that E-selectin plays an important role in the early stage of HSV-1 infection on HDMEC, and that ICAM-1 and VCAM-1 have a similarly important role in the late stages. IL-1a can act on human vascular endothelium and increase the adherence of circulating blood leukocytes to endothelial cells, and thus can induce leukocyte trafficking at sites of inflammation in vivo [18]. TNFa also has a similar effect.…”

Inhalation of swine dust induces cytokine release in the upper and lower airways

“…These cytokines act synergistically on the stimulation of polymorphonuclear neutrophilic granulocyte migration [31], and stimulate vascular endothelial cells to promote transendothelial passage of neutrophils, albumin, and fluid in vitro and in animal experiments [32][33][34]. TNF-α, IL-1 and LPS induce the expression of the adhesion molecules intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and E-selectin on endothelial cells, promoting adhesion to granulocytes, monocytes and lymphocytes [35][36][37][38]. The production of TNF-α and IL-1 in the upper and lower airways could, thus, contribute to the influx of inflammatory cells following exposure.…”

Dietary n-3 polyunsaturated fatty acids prevent the development of atherosclerotic lesions in mice. Modulation of macrophage secretory activities.

“…Indeed, IL-1 induces a variety of responses in endothelial cells, resulting in the stimulation of granulocyte adhesion, 36 an increase in procoagulant activity, 37 and the proliferation of endothelial cells. 38 IL-1 also stimulates the proliferation 39 and secretion 40 of plateletderived growth factor by smooth muscle cells.…”