Miyabayashi M, Yasui K
Department of Pediatrics, Shinshu University School of Medicine, Matsumoto, Japan.
Int J Hematol. 1996 Dec;65(1):49-59. doi: 10.1016/s0925-5710(96)00525-7.
Polymorphonuclear leukocyte-endothelial cell (PMN-EC) adhesion and the O2- production by subsequently triggered polymorphonuclear leukocytes (PMN) must be involved in the development of multiple organ failure at septic inflammatory sites. In this study, the adhesion and O2- production of PMN treated with LPS and serum, were markedly enhanced on the EC monolayer by treatment with TNF-alpha or LPS. However, in the intact EC monolayer, neither adhesion nor O2- production was increased. Monoclonal antibodies (mAb) against CD18, CD11b, and ICAM-1 inhibited PMN-EC adhesion. All antibodies except for anti-CD11b mAb had no effect on O2- production by adhered PMN. Anti-CD11b mAb stimulated O2- production in a PMN cell suspension. The pertussis toxin, an inhibitor of some G-proteins, inhibited this reaction. These findings indicate that the adhesion mediated by CD11b provides the signal for O2- production by PMN. This O2- production may involve a signal transduction mechanism mediated by pertussis toxin-sensitive G-proteins.
多形核白细胞-内皮细胞（PMN-EC）黏附以及随后被触发的多形核白细胞（PMN）产生超氧阴离子（O₂⁻）必定参与了脓毒症炎症部位多器官功能衰竭的发生发展。在本研究中，用脂多糖（LPS）和血清处理的PMN的黏附及O₂⁻产生，经肿瘤坏死因子-α（TNF-α）或LPS处理后在EC单层上显著增强。然而，在完整的EC单层中，黏附及O₂⁻产生均未增加。抗CD18、抗CD11b和抗细胞间黏附分子-1（ICAM-1）单克隆抗体（mAb）抑制PMN-EC黏附。除抗CD11b mAb外，所有抗体对黏附的PMN产生O₂⁻均无影响。抗CD11b mAb在PMN细胞悬液中刺激O₂⁻产生。百日咳毒素，一种某些G蛋白的抑制剂，抑制了该反应。这些发现表明，由CD11b介导的黏附为PMN产生O₂⁻提供了信号。这种O₂⁻产生可能涉及由百日咳毒素敏感的G蛋白介导的信号转导机制。
