Fitzpatrick Leo R, Wang Jian, Le Truc, Calingasan Noel
Gastrointestinal Inflammation Department, Maryland Research Laboratories, Otsuka Maryland Research Institute, Rockville, Maryland 20850, USA.
Dig Dis Sci. 2003 Apr;48(4):775-82. doi: 10.1023/a:1022853213009.
Nuclear factor-kappa B has been proposed to play a role in the pathogenesis of bacterial peptidoglycan-polysaccharide-induced colitis. However, its colonic expression has not been defined in detail. The primary aim of this study was to profile this expression in the rat colon. Peptigoglycan-polysaccharide was administered to the rat colon by direct intramural injections. Gross colonic injury was determined at various time points. Concomitantly, colonic nuclear factor-kappa B was measured by an electrophoretic mobility shift assay and by immunohistochemistry. Gross colonic injury and colonic nuclear factor-kappa B expression showed similar time courses following peptigoglycan-polysaccharide administration. Peak colonic injury and nuclear factor-kappa B expression were found on day 21. Nuclear factor-kappa B was mainly expressed in submucosal inflammatory cells. In conclusion, the administration of bacterial peptidoglycan-polysaccharide to the rat colon caused a chronic colitis, which was characterized by up-regulated colonic nuclear factor-kappa B.
核因子-κB被认为在细菌肽聚糖-多糖诱导的结肠炎发病机制中起作用。然而,其在结肠中的表达尚未得到详细界定。本研究的主要目的是分析其在大鼠结肠中的表达情况。通过直接壁内注射将肽聚糖-多糖注入大鼠结肠。在不同时间点测定结肠大体损伤情况。同时,通过电泳迁移率变动分析和免疫组织化学法检测结肠核因子-κB。给予肽聚糖-多糖后,结肠大体损伤和结肠核因子-κB表达呈现相似的时间进程。在第21天发现结肠损伤和核因子-κB表达达到峰值。核因子-κB主要表达于黏膜下炎症细胞。总之,向大鼠结肠给予细菌肽聚糖-多糖可导致慢性结肠炎,其特征为结肠核因子-κB上调。