Lundin P D, Ekström G, Erlansson M, Lundin S, Weström B R
Dept. of Animal Physiology, Lund University, Sweden.
Scand J Gastroenterol. 1997 Jul;32(7):700-5. doi: 10.3109/00365529708996521.
Since intestinal inflammation is correlated with impaired barrier functions, transgenic HLA-B27/human beta 2-microglobulin rats that spontaneously develop intestinal inflammation were used to investigate whether onset of inflammation or impaired barrier function was the initial event.
During the age period of 9-14 weeks, transgenic and non-transgenic (control) rats were gavaged weekly with the marker molecules, 51Cr-ethylenediaminetetraacetic acid, 1-deamino-8-D-arginine vasopressin, and albumin, which were quantified in blood or urine.
At 12 weeks of age the first signs of inflammation appeared with decreased body weight gain, decreased urine production, and onset of diarrhea. By 14-15 weeks of age all transgenic rats had developed intestinal inflammation, as confirmed by histology and increased myeloperoxidase content, whereas no inflammation was observed in controls. Intestinal passage of the markers did, however, not differ between transgenic and control rats over the studied period.
The results suggest that intestinal inflammation precedes altered intestinal barrier function in this inflammation model.
由于肠道炎症与屏障功能受损相关，因此利用自发发生肠道炎症的转基因HLA - B27/人β2 - 微球蛋白大鼠来研究炎症发作或屏障功能受损是否为初始事件。
在9至14周龄期间，每周给转基因和非转基因（对照）大鼠灌胃标记分子51Cr - 乙二胺四乙酸、1 - 去氨基 - 8 - D - 精氨酸加压素和白蛋白，并对血液或尿液中的这些物质进行定量分析。
12周龄时出现炎症的最初迹象，表现为体重增加减少、尿量减少和腹泻发作。到14至15周龄时，所有转基因大鼠均出现肠道炎症，组织学检查和髓过氧化物酶含量增加证实了这一点，而对照组未观察到炎症。然而，在研究期间，转基因大鼠和对照大鼠之间标记物的肠道通过率并无差异。
结果表明，在该炎症模型中，肠道炎症先于肠道屏障功能改变出现。
