Steroid therapy can modulate gut barrier function, host defense, and survival in thermally injured mice
Steroid therapy can modulate gut barrier function, host defense, and survival in thermally injured mice
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DOI：
10.1006/jsre.1996.0172
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发表时间：
1996-04-01
影响因子：
2.2
通讯作者：
Pyles, T
中科院分区：
文献类型：
--
作者：
Gianotti, L;Alexander, JW;Pyles, T
强的松可能具有免疫抑制作用，而脱氢表雄酮可能刺激免疫反应，但它们对细菌易位引起的肠道源性败血症的影响尚未研究。Balb/c小鼠口服强的松（1或10 mg/kg/天）或生理盐水4天，然后灌胃10(10)c -14标记的大肠杆菌和20%热损伤。小鼠输注同种异体血，皮下注射脱氢表雄酮（5或25 mg/kg/天）或载药4 d，然后进行细菌灌胃和热损伤。在每个实验中，一些组观察10天的死亡率，另一些组在烧伤后4天处死，以测量易位细菌的易位和存活率。泼尼松治疗动物的存活率为25% （10 mg/kg/天）和75% （1 mg/kg/天），而对照组为80%。给予脱氢表雄酮后，存活率为72% （25 mg/kg/天/组）和30% （5 mg/kg/天/组），而对照组为16%。大剂量强的松增加了细菌向肠壁和肠系膜淋巴结的易位，并大大损害了对易位大肠杆菌的杀灭。相反，脱氢表雄酮（25 mg/kg）不影响易位，但显著提高细菌杀灭。强的松和脱氢表雄酮在肠源性败血症中发挥相反的作用。(C) 1996学术出版社，Inc.
Prednisone may be immunosuppressive and dehydroepiandrosterone may stimulate the immune response, but their effect on gut origin sepsis caused by bacterial translocation has not been studied. Balb/c mice were treated orally with prednisone (1 or 10 mg/kg/day) or saline for 4 days before receiving gavage with 10(10) C-14-labeled Escherichia coli and a 20% thermal injury. Mice were transfused with allogeneic blood and given dehydroepiandrosterone (5 or 25 mg/kg/day) or vehicle subcutaneously for 4 days before bacterial gavage and thermal injury. Some groups in each experiment were observed 10 days for mortality and others were sacrificed 4 hi postburn to measure translocation and survival of translocated bacteria, Survival in prednisone treated animals was 25% (10 mg/kg/day) and 75% (1 mg/kg/day) versus 80% for controls. Following dehydroepiandrosterone administration, survival was 72% (25 mg/kg/day/group) and 30% (5 mg/kg/day/group) versus 16% for controls. High dose prednisone increased bacterial translocation to the intestinal wall and mesenteric lymph nodes and greatly impaired killing of translocated E. coli. In contrast, dehydroepiandrosterone (25 mg/kg) did not affect translocation but significantly improved bacterial killing. Prednisone and dehydroepiandrosterone exert opposite effects during gut-derived sepsis. (C) 1996 Academic Press, Inc.