作者: F. W. Luscinskas , M. A. Gimbrone , J. B. Baker , Han Ding , J. M. Kiely
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摘要: We have previously reported that cytokine- or LPS-activated human umbilical vein endothelial cell (HUVEC) monolayers secrete IL-8 can act as a neutrophil-selective adhesion inhibitor. In our study we investigated the mechanisms involved in leukocyte inhibitory action of IL-8. The effect appears to be mediated by on neutrophil, does not involve down-regulation relevant molecules such endothelial-leukocyte molecule-1 intercellular molecule-1, and is quantitatively similar different activation states are predominantly dependent dependent. addition inhibiting attachment freshly isolated peripheral blood neutrophils cytokine-activated HUVEC monolayers, also promoted rapid detachment tightly adherent from activated HUVEC, abolished neutrophil transendothelial migration. Certain other chemoattractants, including FMLP C5a, had actions, indicating was unique its ability inhibit various neutrophil-endothelial interactions. contrast, two agonists 1-0-alkyl-2-acetyl sn-glycero-3-phosphocholine granulocyte-macrophage-CSF, which, like IL-8, produced well leukocyte-derived chemoattractant leukotriene B4, exerted minimal effects adhesion. Regardless their modulate adhesion, all these agents induced altered surface expression functionally important molecules, loss L-selectin (leukocyte LECAM-1) increase CD11b/CD18. Thus, although above been characterized primarily findings demonstrate exert wide range modulatory adhesive