Stanley C M, Phillips T E
Division of Biological Sciences, University of Missouri, Columbia 65211.
Agents Actions. 1994 Oct;42(3-4):141-5. doi: 10.1007/BF01983480.
The effect of the inflammatory mediator bradykinin on glycoprotein synthesis and mucin secretion in the human colonic adenocarcinoma cell line HT29-18N2 was examined. Bradykinin, at a threshold of 0.01 microM, accelerated the rate of mucin discharge as assessed by a mucin-specific ELISA. Using immunofluorescence microscopy, a thick meshwork of extracellular mucus was observed over bradykinin-treated monolayers but not mock-treated controls. Morphometric analysis of bradykinin-treated monolayers revealed no decreases in intracellular mucin stores or any other easily discernable morphological alteration. The ability of the cyclooxygenase inhibitors indomethacin and naproxen to decrease the response to bradykinin by approximately 68% indicates the effect is mediated, at least partially, through the generation of prostaglandins. Bradykinin did not alter the rate of incorporation of 3H-glucosamine into newly synthesized glycoproteins. Bradykinin-accelerated mucin secretion may be linked to the depletion of intracellular mucin stores in the inflammatory bowel disease ulcerative colitis.
研究了炎症介质缓激肽对人结肠腺癌细胞系HT29-18N2中糖蛋白合成和粘蛋白分泌的影响。通过粘蛋白特异性酶联免疫吸附测定法评估，缓激肽在0.01微摩尔的阈值下加速了粘蛋白的释放速率。使用免疫荧光显微镜观察到，在经缓激肽处理的单层细胞上有一层厚厚的细胞外粘液网络，而未经处理的对照则没有。对经缓激肽处理的单层细胞进行形态计量分析，结果显示细胞内粘蛋白储备没有减少，也没有任何其他易于识别的形态学改变。环氧化酶抑制剂吲哚美辛和萘普生使对缓激肽的反应降低约68%，这表明该效应至少部分是通过前列腺素的生成介导的。缓激肽没有改变3H-葡萄糖胺掺入新合成糖蛋白的速率。缓激肽加速的粘蛋白分泌可能与炎症性肠病溃疡性结肠炎中细胞内粘蛋白储备的消耗有关。
