Li M, Specian R D, Berg R D, Deitch E A
Department of Surgery, Louisiana State University School of Medicine, Shreveport 71130-3932.
JPEN J Parenter Enteral Nutr. 1989 Nov-Dec;13(6):572-8. doi: 10.1177/0148607189013006572.
Since protein malnourished or endotoxemic patients are at increased risk of developing nosocomial infections with enteric organisms, we investigated the effects of these risk factors alone and in combination on the intestinal mucosal barrier to bacteria. Protein malnutrition resulted in severe ileal atrophy that was directly related to the length of time the mice were protein malnourished. Although protein malnutrition did not promote bacterial translocation from the gut to systemic organs, the protein-malnourished mice were more susceptible to endotoxin-induced bacterial translocation than normally nourished mice (p less than 0.01). Since the gross epithelial damage documented after endotoxin administration in normally nourished mice was diminished after protein malnutrition, there was no correlation between the gross appearance of the epithelial mucosal barrier and the extent of endotoxin-induced bacterial translocation. These results suggest that the synergistic effect of endotoxin plus protein malnutrition on bacterial translocation is not primarily related to failure of the gut mucosal barrier. Nonetheless, it appears that protein-malnourished mice are less able to clear translocating bacteria than normally nourished mice.
由于蛋白质营养不良或内毒素血症患者发生肠道微生物引起的医院感染的风险增加,我们研究了这些风险因素单独及联合作用对肠道细菌黏膜屏障的影响。蛋白质营养不良导致严重的回肠萎缩,这与小鼠蛋白质营养不良的时间长短直接相关。虽然蛋白质营养不良不会促进细菌从肠道向全身器官的移位,但与正常营养的小鼠相比,蛋白质营养不良的小鼠对内毒素诱导的细菌移位更敏感(p小于0.01)。由于正常营养的小鼠在内毒素给药后记录的明显上皮损伤在蛋白质营养不良后减轻,上皮黏膜屏障的外观与内毒素诱导的细菌移位程度之间没有相关性。这些结果表明,内毒素加蛋白质营养不良对细菌移位的协同作用并非主要与肠道黏膜屏障功能衰竭有关。尽管如此,蛋白质营养不良的小鼠清除移位细菌的能力似乎低于正常营养的小鼠。