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内毒素而非营养不良会促进烧伤小鼠肠道菌群的细菌移位。

Endotoxin but not malnutrition promotes bacterial translocation of the gut flora in burned mice.

作者信息

Deitch E A, Berg R D

出版信息

J Trauma. 1987 Feb;27(2):161-6. doi: 10.1097/00005373-198702000-00012.

DOI:10.1097/00005373-198702000-00012
PMID:2950241
Abstract

Previously we have shown that under certain conditions, bacteria can pass through the intact epithelial mucosa to the mesenteric lymph nodes (MLN), liver, spleen, and bloodstream to cause infection, a process termed bacterial translocation. To extend these studies, we determined the influence of protein malnutrition and endotoxemia on bacterial translocation in burned (25% TBSA) and unburned mice. The results of these experiments documented that protein malnutrition did not promote bacterial translocation from the gut in either burned or unburned animals, although it did disrupt the normal indigenous gut flora. In contrast, a nonlethal dose of endotoxin (IP) promoted bacterial translocation to the mesenteric lymph nodes in burned and unburned mice, but only in burned mice did the bacteria translocate from the gut to other systemic organs (p less than 0.01). Furthermore, the mortality rate of mice receiving only endotoxin or burn was less than 10%, while the combination of endotoxin plus a thermal injury increased the mortality rate to 100% (p less than 0.01). These studies support the concept that bacteria may translocate from the gut to other organs and be a potential source of lethal infections after thermal injury.

摘要

此前我们已经表明,在某些条件下,细菌可穿过完整的上皮黏膜到达肠系膜淋巴结(MLN)、肝脏、脾脏和血液中引发感染,这一过程被称为细菌移位。为了拓展这些研究,我们测定了蛋白质营养不良和内毒素血症对烧伤(25%体表面积)及未烧伤小鼠细菌移位的影响。这些实验结果表明,蛋白质营养不良在烧伤或未烧伤动物中均未促进肠道细菌移位,尽管它确实破坏了正常的肠道固有菌群。相比之下,非致死剂量的内毒素(腹腔注射)促进了烧伤和未烧伤小鼠肠道细菌移位至肠系膜淋巴结,但只有烧伤小鼠中的细菌从肠道移位至其他全身器官(p<0.01)。此外,仅接受内毒素或烧伤的小鼠死亡率低于10%,而内毒素加热力损伤的联合作用使死亡率增至100%(p<0.01)。这些研究支持了这样一种观点,即细菌可能从肠道移位至其他器官,并成为热力损伤后致死性感染的潜在来源。

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Endotoxin but not malnutrition promotes bacterial translocation of the gut flora in burned mice.内毒素而非营养不良会促进烧伤小鼠肠道菌群的细菌移位。
J Trauma. 1987 Feb;27(2):161-6. doi: 10.1097/00005373-198702000-00012.
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