Oshima S, Fujimura M, Fukimiya M
Department of Second Surgery, Shiga University of Medical Science, Seta, Otsu, Shiga 520-21, Japan.
Histochem Cell Biol. 1999 Oct;112(4):257-63. doi: 10.1007/s004180050445.
The role of serotonin in the pathogenesis of inflammatory bowel disease has not been fully studied. We examined the changes in the serotonin level and the density of serotonin-containing enterochromaffin (EC) and mast cells in the intestinal mucosa of dextran sodium sulfate (DSS)-induced colitis in rats. Rats were treated with 1.5% DSS for 1 month. Serotonin levels were biochemically measured and the density of epithelial EC cells and mucosal mast cells was quantified by serotonin immunohistochemistry. DSS caused malnutrition due to chronic diarrhea. Infiltrated inflammatory cells were microscopically observed in the colonic wall with intact epithelium. The serotonin content in the mucosa/submucosa tissue was increased in the proximal and distal colon in DSS-treated rats, compared to that in control rats. The density of EC cells in the epithelium also increased in the proximal and distal colon in DSS-treated rats. In contrast, the density of mast cells in the lamina propria dramatically increased in the distal, but not in the proximal colon in DSS-treated rats. This discrepancy implies the serotonin released from EC cells and from mast cells may play different roles in the pathogenesis of DSS-induced colitis.
血清素在炎症性肠病发病机制中的作用尚未得到充分研究。我们检测了葡聚糖硫酸钠(DSS)诱导的大鼠结肠炎肠黏膜中血清素水平以及含血清素的肠嗜铬(EC)细胞和肥大细胞密度的变化。大鼠用1.5% DSS处理1个月。通过生化方法测定血清素水平,并通过血清素免疫组织化学对上皮EC细胞和黏膜肥大细胞的密度进行定量。DSS由于慢性腹泻导致营养不良。在结肠壁中可镜下观察到有浸润的炎症细胞,上皮完整。与对照大鼠相比,DSS处理大鼠近端和远端结肠黏膜/黏膜下层组织中的血清素含量增加。DSS处理大鼠近端和远端结肠上皮中EC细胞的密度也增加。相比之下,DSS处理大鼠远端结肠固有层中肥大细胞的密度显著增加,而近端结肠则未增加。这种差异表明,EC细胞和肥大细胞释放的血清素可能在DSS诱导的结肠炎发病机制中发挥不同作用。