Tanaka Y, Kobayashi K, Takahashi A, Arai I, Higuchi S, Otomo S, Habu S, Nishimura T
Department of Pharmacology, Taisho Pharmaceutical Co., Ltd., Ohmiya, Japan.
J Immunol. 1993 Nov 1;151(9):5088-95.
When mice were given an i.v. injection of LPS 7 days after an i.v. injection of Propionibacterium acnes, liver injury and a rapid increase of serum alanine aminotransferase and asparagine acid aminotransferase occurred. The in vivo administration of mAb against LFA-1 on days 1, 2, and 3 after the i.v. injection of P. acnes resulted in a potent inhibition of all these dysfunctions. Using P. acnes and the LPS model, we found that anti-LFA-1 mAb protected the mice from P. acnes and LPS-induced lethal shock. During the course of P. acnes and LPS-induced liver injury, inflammatory cells infiltrated the liver and caused a massive hepatic cell necrosis. Flow cytometry revealed that the liver-infiltrating cells were mainly leukocytes expressing a higher level of LFA-1 antigen than that seen in the normal liver. These results suggested that the LFA-1 molecule on liver-infiltrating leukocytes may play an important role in the induction of inflammatory liver injury.
在静脉注射痤疮丙酸杆菌7天后给小鼠静脉注射脂多糖（LPS），会出现肝损伤以及血清丙氨酸转氨酶和天冬氨酸转氨酶迅速升高的情况。在静脉注射痤疮丙酸杆菌后的第1、2和3天，体内给予抗淋巴细胞功能相关抗原-1（LFA-1）单克隆抗体（mAb）可有效抑制所有这些功能障碍。利用痤疮丙酸杆菌和LPS模型，我们发现抗LFA-1 mAb可保护小鼠免受痤疮丙酸杆菌和LPS诱导的致死性休克。在痤疮丙酸杆菌和LPS诱导的肝损伤过程中，炎症细胞浸润肝脏并导致大量肝细胞坏死。流式细胞术显示，肝脏浸润细胞主要是白细胞，其表达的LFA-1抗原水平高于正常肝脏中的白细胞。这些结果表明，肝脏浸润白细胞上的LFA-1分子可能在炎症性肝损伤的诱导中起重要作用。
