Deitch E A, Berg R, Specian R
Arch Surg. 1987 Feb;122(2):185-90. doi: 10.1001/archsurg.1987.01400140067008.
Experiments were performed in mice to determine whether endotoxin could cause bacteria normally colonizing the gut to spread systemically, a process termed bacterial translocation. Endotoxin given intraperitoneally promoted bacterial translocation in a dose-dependent fashion from the gut to the mesenteric lymph node (MLN). The incidence of bacterial translocation to the MLN was similar whether the endotoxin was administered intramuscularly or intraperitoneally, although the number of bacteria colonizing the MLN was greater with intraperitoneal endotoxin. The incidence and magnitude of endotoxin-induced bacterial translocation were similar between CD-1 and C3H/HeJ (endotoxin-resistant) mice, indicating that bacterial translocation is not prevented by genetic resistance to endotoxin. Thus, it appears that the gut may serve as a reservoir for bacteria causing systemic infections during endotoxemia.
在小鼠身上进行了实验,以确定内毒素是否会导致通常定植于肠道的细菌发生全身扩散,这一过程称为细菌移位。腹腔注射内毒素以剂量依赖的方式促进细菌从肠道向肠系膜淋巴结(MLN)移位。无论内毒素是肌肉注射还是腹腔注射,细菌移位至MLN的发生率相似,尽管腹腔内注射内毒素时定植于MLN的细菌数量更多。CD-1小鼠和C3H/HeJ(对内毒素耐受)小鼠在内毒素诱导的细菌移位的发生率和程度方面相似,这表明对内毒素的遗传抗性并不能阻止细菌移位。因此,似乎肠道可能是内毒素血症期间引起全身感染的细菌的储存库。