Hutto D L, Wannemuehler M J
Department of Veterinary Pathology, College of Veterinary Medicine, Iowa State University, Ames 50010, USA.
Vet Pathol. 1999 Sep;36(5):412-22. doi: 10.1354/vp.36-5-412.
Studies were carried out to compare the early morphologic changes in the cecal mucosa of mice either infected with Serpulina hyodysenteriae or exposed to the beta-hemolysin of S. hyodysenteriae. Sixty-five 12-24-week-old C3H/HeOuJ mice were infected with S. hyodysenteriae by gastric intubation. Two mice were necropsied every hour for 30 hours following infection. S. hyodysenteriae was isolated from the cecal contents of each mouse at all time points. Macroscopic lesions were first apparent at 14 hours postinfection (PI), and light microscopic lesions were first apparent at 10 hours PI, earlier than has been previously reported. Ultrastructural changes, first evident at 6 hours PI, included disarray and loss of microvilli and terminal web, with dilatation of intercellular spaces. Luminal bacteria were translocated through epithelial cells to the lamina propria, where capillaries exhibited changes indicative of increased permeability. In another experiment, solutions containing between 2,500 and 25,000 hemolytic units of purified S. hyodysenteriae hemolysin were placed within the lumen of surgically closed murine ceca (n = 10); ceca were collected for examination 3 hours following treatment. Ultrastructural changes consisted of loss of microvilli and terminal web and marked vacuolation and exfoliation of epithelial cells. Significant numbers of necrotic and apoptotic epithelial cells were present, and epithelial cells internalized moderate numbers of bacteria. The hemolysin of S. hyodysenteriae induces some of the same early ultrastructural changes in the cecal epithelium of mice as occur following infection with S. hyodysenteriae. Based on the observed bacterial translocation, luminal bacteria also appear to play a unique role in lesion development in this model.
开展了多项研究,以比较感染猪痢疾蛇形螺旋体或暴露于猪痢疾蛇形螺旋体β-溶血素的小鼠盲肠黏膜的早期形态学变化。通过胃内插管法,将65只12 - 24周龄的C3H/HeOuJ小鼠感染猪痢疾蛇形螺旋体。感染后30小时内,每小时剖检2只小鼠。在所有时间点,均从每只小鼠的盲肠内容物中分离出猪痢疾蛇形螺旋体。肉眼可见的病变在感染后14小时首次出现,光学显微镜下的病变在感染后10小时首次出现,比先前报道的时间更早。超微结构变化在感染后6小时首次显现,包括微绒毛和终末网紊乱及缺失,细胞间隙扩张。肠腔内细菌通过上皮细胞转移至固有层,固有层中的毛细血管出现通透性增加的变化。在另一项实验中,将含有2500至25000个溶血单位纯化猪痢疾蛇形螺旋体溶血素的溶液置于手术封闭的小鼠盲肠腔内(n = 10);处理3小时后收集盲肠进行检查。超微结构变化包括微绒毛和终末网缺失,上皮细胞出现明显空泡化和脱落。存在大量坏死和凋亡的上皮细胞,上皮细胞内化了中等数量的细菌。猪痢疾蛇形螺旋体的溶血素在小鼠盲肠上皮细胞中诱导出一些与感染猪痢疾蛇形螺旋体后相同的早期超微结构变化。基于观察到的细菌转移现象,肠腔内细菌在该模型的病变发展中似乎也起着独特作用。