Bird J, Tissot M, Giroud J P
Agents Actions. 1985 Dec;17(2):184-91. doi: 10.1007/BF01966590.
The chemiluminescent (CL) response of peritoneal macrophages was suppressed by induction 4 h earlier of an inflammatory reaction in the pleural cavity which was negated by prior administration of indomethacin, ketoprofen and BW 755C. These changes were accompanied by a concomitant rise in peritoneal PGI2 levels which was abolished by drug pretreatment. In vitro treatment of normal peritoneal macrophages with PGI2 inhibited their subsequent CL response. Indomethacin and ketoprofen produced elevated CL of macrophages obtained from untreated controls in vitro which was blocked by the lipoxygenase inhibitor NDGA. BW 755C and NDGA in vitro strongly inhibited macrophage CL and partially inhibited CL in a cell-free system. Use of these drugs in vivo demonstrated that indomethacin and ketoprofen augmented the CL response of peritoneal macrophages while BW 755C had no effect. These results suggest the inflammatory process per se can modulate the functions of macrophages in parts of the body remote from the inflammatory site. Moreover this modulation may be under the control of the prostanoid system.
胸腔炎症反应提前4小时诱导可抑制腹腔巨噬细胞的化学发光（CL）反应，而吲哚美辛、酮洛芬和BW 755C预先给药可消除这种抑制作用。这些变化伴随着腹腔PGI2水平的相应升高，药物预处理可消除这种升高。用PGI2体外处理正常腹腔巨噬细胞可抑制其随后的CL反应。吲哚美辛和酮洛芬可使体外从未经处理的对照中获得的巨噬细胞CL升高，这种升高被脂氧合酶抑制剂NDGA阻断。BW 755C和NDGA在体外强烈抑制巨噬细胞CL，并在无细胞系统中部分抑制CL。体内使用这些药物表明，吲哚美辛和酮洛芬增强了腹腔巨噬细胞的CL反应，而BW 755C没有作用。这些结果表明，炎症过程本身可调节远离炎症部位的身体其他部位巨噬细胞的功能。此外，这种调节可能受前列腺素系统的控制。
