Chiu Chien-Chao, Huang Yen-Te, Chuang Hsiao-Li, Chen Hans Hsien-Chuan, Chung Tung-Ching
Department of Veterinary Medicine, National Chung Hsing University, Taichung, Taiwan.
Immunopharmacol Immunotoxicol. 2009;31(1):75-82. doi: 10.1080/08923970802357724.
Pseudomonas aeruginosa Exotoxin A (PEA) induces hepatotoxicity in experimental animals. Lipopolysaccharide (LPS) interacts synergistically with xenotoxics to induce severe organ injury. We examined the combination of non-injurious doses of LPS and sub-hepatotoxic PEA in the induction of multiple organ injury (MOI). Rats treated with 20 or 40 microg/kg LPS plus 10 microg/kg PEA developed severe liver, kidney, and lung injury; elevation of TNF-alpha, IFN-gamma, and IL-2; and high mortality. Depletion of Kupffer cells or T-cells by pretreatment with Gadolinium Chloride or FK506, respectively, attenuated MOI. Thus LPS + PEA acted synergistically on Kupffer and T-cells to induce proinflammatory cytokines contributing to MOI.
铜绿假单胞菌外毒素A（PEA）可在实验动物中诱发肝毒性。脂多糖（LPS）与外源性毒素协同作用可诱发严重的器官损伤。我们研究了无损伤剂量的LPS与亚肝毒性剂量的PEA联合使用对多器官损伤（MOI）的诱导作用。用20或40微克/千克LPS加10微克/千克PEA处理的大鼠出现了严重的肝、肾和肺损伤；肿瘤坏死因子-α、干扰素-γ和白细胞介素-2水平升高；且死亡率很高。分别用氯化钆或FK506预处理使库普弗细胞或T细胞耗竭，可减轻多器官损伤。因此，LPS + PEA对库普弗细胞和T细胞起协同作用，诱导促炎细胞因子，从而导致多器官损伤。
