Yamaguchi M, Machida H, Korenaga R, Toyama-Sorimachi N, Ando J, Miyasaka M, Matsumoto T, Nakano H, Kumada K, Takeda M
Department of Surgery, Showa University Fujigaoka Hospital, Yokohama, Japan.
Surg Today. 1999;29(9):966-9. doi: 10.1007/BF02482799.
Leukocyte-vascular endothelial cell (EC) interactions which promote inflammatory and immune reactions involve bidirectional signaling between two cell types. We investigated the effects of flow on neutrophil-mediated changes in endothelial intracellular Ca2+ levels ([Ca2+]i). Cultured human umbilical vein ECs stimulated by endotoxin were labeled with Fura-2 and exposed to fluid flow with neutrophils. The individual changes in [Ca2+]i were monitored. The application of flow with neutrophils to stimulated ECs led to an increase in [Ca2+]i although either flow without neutrophils or neutrophils without flow rarely induced a rise in [Ca2+]i. Furthermore, flow application with neutrophils to unstimulated ECs also rarely promoted a rise in [Ca2+]i. These findings suggest that the flow might thus induce or enhance the inflammatory process by the induction of Ca2+ signaling in endotoxin-stimulated endothelium facing neutrophils in the blood flow.
促进炎症和免疫反应的白细胞与血管内皮细胞（EC）相互作用涉及两种细胞类型之间的双向信号传导。我们研究了血流对中性粒细胞介导的内皮细胞内钙离子水平（[Ca2+]i）变化的影响。用Fura-2标记受内毒素刺激的培养人脐静脉内皮细胞，并使其暴露于含有中性粒细胞的流体流动中。监测[Ca2+]i的个体变化。将含有中性粒细胞的血流施加于受刺激的内皮细胞会导致[Ca2+]i升高，而单独的无中性粒细胞的血流或无血流的中性粒细胞很少能诱导[Ca2+]i升高。此外，将含有中性粒细胞的血流施加于未受刺激的内皮细胞也很少能促进[Ca2+]i升高。这些发现表明，血流可能通过在内毒素刺激的、面对血流中中性粒细胞的内皮细胞中诱导钙离子信号传导来诱导或增强炎症过程。
