Giannella R A, Rout W R, Formal S B, Collins H
Infect Immun. 1976 Feb;13(2):470-4. doi: 10.1128/iai.13.2.470-474.1976.
The mechanisms whereby invasive enteropathogens, e.g., Salmonella typhimurium, induce intestinal secretion are largely unknown. Since these organisms penetrate the intestinal epithelium, disrupt the brush border, and evoke an acute inflammatory reaction, increased plasma filtration through a damaged, more permeable epithelium might contribute to the secretory process. To examine this possibility, the plasma-to-lumen clearance of two different sized molecules, [51Cr]albumin and [14C]mannitol, was measured in the in vivo rabbit ileal loop and in vivo rhesus monkey models of salmonellosis. In the rabbit ileal loop model, the clearance of neither molecule was increased when compared to cholera toxin-exposed loops. In the rhesus monkey, clearance of [14C]mannitol into the jejunum, ileum, and colon of Salmonella-infected animals did not differ from the observed in control animals. These data indicate that invasion of the intestinal mucosa by S. typhimurium has not substantially altered the permeability characteristics of the intestinal mucosa and that plasma filtration through a damaged, more permeable mucosa does not contribute to the Salmonella-induced intestinal secretory process.
侵袭性肠道病原体,如鼠伤寒沙门氏菌,引发肠道分泌的机制在很大程度上尚不清楚。由于这些病原体穿透肠上皮,破坏刷状缘,并引发急性炎症反应,通过受损且通透性更高的上皮进行的血浆滤过增加可能有助于分泌过程。为了检验这种可能性,在兔回肠袢体内模型和恒河猴沙门氏菌病体内模型中,测量了两种不同大小分子[51Cr]白蛋白和[14C]甘露醇从血浆到肠腔的清除率。在兔回肠袢模型中,与暴露于霍乱毒素的肠袢相比,两种分子的清除率均未增加。在恒河猴中,感染沙门氏菌的动物空肠、回肠和结肠中[14C]甘露醇的清除率与对照动物中观察到的无差异。这些数据表明,鼠伤寒沙门氏菌对肠黏膜的侵袭并未显著改变肠黏膜的通透性特征,且通过受损且通透性更高的黏膜进行的血浆滤过对沙门氏菌诱导的肠道分泌过程没有作用。