Osman N E, Weström B, Karlsson B
Dept. of Animal Physiology, Lund University, Sweden.
Scand J Gastroenterol. 1998 Nov;33(11):1170-4. doi: 10.1080/00365529850172520.
Microbial endotoxins are normally present in the gut, usually without apparent harmful effects, whereas systemically administered endotoxin impairs the mucosal barrier function. Our aim was to investigate whether in vitro exposure to bacterial lipopolysaccharide (LPS) could affect the intestinal barrier properties of the rat small intestine.
Small-intestinal segments from rats were mounted in Ussing diffusion chambers, and the mucosal to serosal permeation of the marker molecules bovine serum albumin (BSA) and 51Cr-ethylenediaminetetraacetic acid (EDTA) was measured after addition of LPS to the mucosal or serosal side.
Mucosal exposure to LPS (0.01, 0.05, 0.25 mg/ml) had no effects on the permeation of BSA and 51Cr-EDTA, whereas when added to the serosal side at 0.05 or 0.25 mg/ml, LPS increased the marker permeation.
Serosal LPS exposure in vitro increased the intestinal permeability to the different-sized markers, whereas mucosal LPS did not, indicating that the mechanisms leading to intestinal barrier impairment can be initiated in the intestinal wall itself.
微生物内毒素通常存在于肠道中，通常无明显有害影响，而全身给予内毒素会损害黏膜屏障功能。我们的目的是研究体外暴露于细菌脂多糖（LPS）是否会影响大鼠小肠的肠道屏障特性。
将大鼠的小肠段安装在尤斯扩散池中，在向黏膜侧或浆膜侧添加LPS后，测量标记分子牛血清白蛋白（BSA）和51铬 - 乙二胺四乙酸（EDTA）从黏膜到浆膜的渗透情况。
黏膜暴露于LPS（0.01、0.05、0.25 mg/ml）对BSA和51铬 - EDTA的渗透无影响，而当以0.05或0.25 mg/ml添加到浆膜侧时，LPS增加了标记物的渗透。
体外浆膜暴露于LPS增加了肠道对不同大小标记物的通透性，而黏膜暴露于LPS则没有，这表明导致肠道屏障受损的机制可能在肠壁自身启动。
