Víctor V M, De la Fuente M
Department of Animal Physiology, Complutense University, Madrid, Spain.
Physiol Res. 2003;52(6):789-96.
We have studied natural killer (NK) activity, lymphoproliferative response, the release of several cytokines (IL-2, TNF alpha and IL-1 beta) and the ROS production in peritoneal leukocytes obtained 0, 2, 4, 12 and 24 h after lipopolysaccharide (LPS) injection. Lethal septic shock (100 % mortality occurred at 30 h after LPS administration) was caused in female BALB/c mice by intraperitoneal injection of 100 mg/kg of E. coli LPS. Cytotoxicity and lymphoproliferation assay were preformed together with the measurement of IL-1 beta, IL-2 and TNF alpha production, and quantification of ROS. Natural killer activity, spontaneous lymphoproliferative response, IL-2, TNF alpha, IL-beta release and ROS production were increased after LPS injection. In conclusions, ROS and proinflammatory mediators produced by immune cells in response to LPS are involved in the oxidative stress of endotoxic shock. This oxidative state alters some functional characteristics of leukocytes (proliferation and NK activity).
我们研究了脂多糖（LPS）注射后0、2、4、12和24小时获取的腹膜白细胞中的自然杀伤（NK）活性、淋巴细胞增殖反应、几种细胞因子（IL-2、TNFα和IL-1β）的释放以及活性氧（ROS）的产生。通过腹腔注射100mg/kg的大肠杆菌LPS，在雌性BALB/c小鼠中引发致死性脓毒症休克（LPS给药后30小时死亡率达100%）。进行细胞毒性和淋巴细胞增殖测定，同时测量IL-1β、IL-2和TNFα的产生以及ROS的定量。LPS注射后，自然杀伤活性、自发淋巴细胞增殖反应、IL-2、TNFα、IL-β释放和ROS产生均增加。总之，免疫细胞对LPS反应产生的ROS和促炎介质参与了内毒素休克的氧化应激。这种氧化状态改变了白细胞的一些功能特性（增殖和NK活性）。
