Yoshida N, Takemura T, Granger D N, Anderson D C, Wolf R E, McIntire L V, Kvietys P R
Department of Physiology, Louisiana State University Medical Center, Shreveport.
Gastroenterology. 1993 Sep;105(3):715-24. doi: 10.1016/0016-5085(93)90888-j.
Previous studies indicate that aspirin can promote neutrophil adhesion to venular endothelium in vivo. The objectives of the present study were (1) to identify the leukocyte and endothelial cell surface glycoproteins that mediate this adhesive interaction and (2) to assess the role of lipoxygenase products, prostanoids, and platelet activating factor in aspirin-induced neutrophil adhesion.
Human neutrophils (polymorphonuclear leukocytes [PMN]) were added to confluent monolayers of human umbilical vein endothelial cells (HUVEC) and coincubated with or without aspirin (30, 150, or 300 micrograms/mL).
Aspirin increased neutrophil adherence to HUVEC in a dose-dependent manner. Pretreatment of HUVEC with aspirin had no effect on PMN adherence whereas pretreatment of PMN significantly increased adherence to HUVEC. Incubation of neutrophils with aspirin increased surface expression of CD11b and CD18 on neutrophils. The aspirin-induced increase in PMN adherence to HUVEC was significantly reduced by monoclonal antibodies against CD18, CD11b, CD11a, and intercellular adhesion molecule 1. Aspirin-induced neutrophil adhesion was diminished by treatment with either a lipoxygenase inhibitor or a leukotriene B4 (LTB4) receptor antagonist.
These studies indicate that aspirin promotes neutrophil adherence to endothelium via CD11a/CD18- and CD11b/CD18-dependent interactions with intercellular adhesion molecule 1; the adhesion response is partially mediated by leukotriene B4.
先前的研究表明阿司匹林可在体内促进中性粒细胞与小静脉内皮细胞的黏附。本研究的目的是：（1）鉴定介导这种黏附相互作用的白细胞和内皮细胞表面糖蛋白；（2）评估脂氧合酶产物、前列腺素和血小板活化因子在阿司匹林诱导的中性粒细胞黏附中的作用。
将人中性粒细胞（多形核白细胞[PMN]）加入人脐静脉内皮细胞（HUVEC）的融合单层中，并在有或无阿司匹林（30、150或300微克/毫升）的情况下共同孵育。
阿司匹林以剂量依赖性方式增加中性粒细胞对HUVEC的黏附。用阿司匹林预处理HUVEC对PMN黏附无影响，而预处理PMN则显著增加其对HUVEC的黏附。用阿司匹林孵育中性粒细胞可增加中性粒细胞表面CD11b和CD18的表达。抗CD18、CD11b、CD11a和细胞间黏附分子1的单克隆抗体可显著降低阿司匹林诱导的PMN对HUVEC黏附的增加。用脂氧合酶抑制剂或白三烯B4（LTB4）受体拮抗剂处理可减少阿司匹林诱导的中性粒细胞黏附。
这些研究表明，阿司匹林通过与细胞间黏附分子1的CD11a/CD18和CD11b/CD18依赖性相互作用促进中性粒细胞与内皮细胞的黏附；黏附反应部分由白三烯B4介导。
