Dobrina A, Carlos T M, Schwartz B R, Beatty P G, Ochs H D, Harlan J M
Institute of General Pathology, University of Trieste, Italy.
Immunology. 1990 Mar;69(3):429-34.
Neutrophils adhere to interleukin-1 (IL-1)-, tumour necrosis factor (TNF)- or lipopolysaccharide (LPS)-pretreated human umbilical vein endothelial cells (HEC) by CD11/CD18-dependent and independent mechanisms. We investigated CD11/CD18-independent neutrophil adherence to LPS-pretreated HEC by: (i) pretreating neutrophils with the anti-CD18 monoclonal antibody mAb 60.3; (ii) performing assays in the absence of Mg2; or (iii) using neutrophils isolated from a patient with leucocyte adhesion deficiency (CD11/CD18-deficiency). Under each of these conditions, CD11/CD18-independent neutrophil adherence to LPS-pretreated HEC was significantly greater than adherence to untreated HEC (15-18% versus 3-7%). In each case, however, stimulation of neutrophils with phorbol ester (PMA) abolished CD11/CD18-independent adherence to LPS-pretreated HEC (less than 5% adherence). Stimulation of neutrophils with bacterial chemotactic peptide (FMLP) or calcium ionophore (A23187) likewise reduced CD18-independent adherence to LPS-pretreated HEC. PMA also inhibited CD11/CD18-independent neutrophil adherence to HEC pretreated with IL-1 or TNF (80-90% inhibition). In contrast, PMA markedly enhanced CD11/CD18-dependent adherence to untreated or LPS-treated HEC. We conclude that stimulation of neutrophils with phorbol ester or other direct agonists down-regulates the CD11/CD18-independent mechanism of neutrophil adherence to IL-1, TNF- or LPS-pretreated HEC.
中性粒细胞通过CD11/CD18依赖和非依赖机制黏附于白细胞介素-1（IL-1）、肿瘤坏死因子（TNF）或脂多糖（LPS）预处理的人脐静脉内皮细胞（HEC）。我们通过以下方式研究了中性粒细胞对LPS预处理的HEC的CD11/CD18非依赖黏附：（i）用抗CD18单克隆抗体mAb 60.3预处理中性粒细胞；（ii）在无Mg2的情况下进行检测；或（iii）使用从白细胞黏附缺陷（CD11/CD18缺陷）患者分离的中性粒细胞。在这些条件下，中性粒细胞对LPS预处理的HEC的CD11/CD18非依赖黏附均显著高于对未处理的HEC的黏附（15 - 18%对3 - 7%）。然而，在每种情况下，用佛波酯（PMA）刺激中性粒细胞均可消除对LPS预处理的HEC的CD11/CD18非依赖黏附（黏附率低于5%）。用细菌趋化肽（FMLP）或钙离子载体（A23187）刺激中性粒细胞同样可降低对LPS预处理的HEC的CD18非依赖黏附。PMA也抑制中性粒细胞对IL-1或TNF预处理的HEC的CD11/CD18非依赖黏附（抑制率80 - 90%）。相反，PMA显著增强对未处理或LPS处理的HEC的CD11/CD18依赖黏附。我们得出结论，用佛波酯或其他直接激动剂刺激中性粒细胞可下调中性粒细胞对IL-1、TNF或LPS预处理的HEC的CD11/CD18非依赖黏附机制。
