Oryu M, Sakamoto H, Ogawa Y, Tanaka S, Sakamoto N
Department of Hospital Pathology, Kagawa Medical School, Japan.
J Leukoc Biol. 1996 Jul;60(1):77-80. doi: 10.1002/jlb.60.1.77.
In this study, the effects of platelet release products (PRPr), ATP, and ADP on the adhesion of human neutrophils to human umbilical vein endothelial cells (HUVEC) and nylon fibers (NF) are described and the implications of various adhesion molecules are considered. Adhesion of neutrophils to HUVEC and NF was increased by PRPr, ATP, and ADP, while their adhesion-increasing actions were cancelled or considerably repressed by apyrase treatment. When anti-CD11a or anti-CD11b was added to neutrophils with PRPr, ATP, or ADP, the adhesion-increasing action was cancelled or considerably repressed. On the other hand, anti-ICAM-1 and anti-CD35 had no significant effects on this action. The above results indicated that platelets, through ATP and ADP in PRPr, increased the adhesion of neutrophils to endothelial cells and foreign bodies. Although it was suggested that the adhesion-increasing action was at least partially based on CD11a and CD11b, ICAM-1 and CD35 had no part in the enhancement of the adhesion.
在本研究中，描述了血小板释放产物（PRPr）、ATP和ADP对人中性粒细胞与人脐静脉内皮细胞（HUVEC）及尼龙纤维（NF）黏附的影响，并探讨了各种黏附分子的作用。PRPr、ATP和ADP可增加中性粒细胞与HUVEC及NF的黏附，而其黏附增强作用可被腺苷三磷酸双磷酸酶处理消除或显著抑制。当将抗CD11a或抗CD11b添加到含有PRPr、ATP或ADP的中性粒细胞中时，黏附增强作用被消除或显著抑制。另一方面，抗ICAM-1和抗CD35对此作用无显著影响。上述结果表明，血小板通过PRPr中的ATP和ADP增加了中性粒细胞与内皮细胞及异物的黏附。虽然提示黏附增强作用至少部分基于CD11a和CD11b，但ICAM-1和CD35在黏附增强过程中不起作用。
