Dwinell M B, Wise R M, Bass P, Oaks J A
Department of Comparative Biosciences, School of Veterinary Medicine, University of Wisconsin, Madison 53706, USA.
Exp Parasitol. 1998 May;89(1):92-102. doi: 10.1006/expr.1998.4271.
The mechanisms mediating motility changes during noninvasive tapeworm infection have not been characterized. In contrast, host intestinal motility changes during invasive nematode infection are mediated by mucosal mast cells (MMC). The purpose of this study was to examine and the correlate onset of myoelectric alterations 8 days after initial tapeworm infection with changes in intestinal morphology, MMC numbers, and MMC secretory activity. Segments of the small intestine, the tapeworms normal habitat, along with stomach, colon, and bladder were taken from tapeworm-infected and control rats. Tissues were fixed and stained to identify MMC and for morphologic measurement. Tapeworm-infected and uninfected rats with chronically implanted intestinal electrodes were treated with ketotifen, a mast cell stabilizer, and in vivo myoelectric activity monitored. In tapeworm-infected rats, the muscularis externa, on day 20 postinfection, and crypts of Lieberkuhn, on day 26 postinfection, from the entire small intestine appeared thickened or deeper, respectively. Increased muscularis thickness was due to smooth muscle hypertrophy in both the circular and the longitudinal muscle layers. Mucosal mastocytosis was first observed on day 26 postinfection and occurred only in the ileum of tapeworm-infected rats. Pharmacologic stabilization of mast cells with ketotifen did not prevent onset of enteric myoelectric alterations during tapeworm infection. Stomach, colon, and bladder MMC numbers and tissue dimensions were not different between Hymenolepis diminuta-infected rats and uninfected controls. Initiation of myoelectric alterations 8 days after infection precedes and may be a contributing factor to the onset of both smooth muscle hypertrophy and mucosal mastocytosis. Taken together, our data indicate that mast cells are not an initiating factor nor chronic stimulus maintaining intestinal myoelectric alterations during H. diminuta infection.
介导非侵袭性绦虫感染期间运动变化的机制尚未明确。相比之下，侵袭性线虫感染期间宿主肠道运动变化是由黏膜肥大细胞（MMC）介导的。本研究的目的是检查并关联初次感染绦虫8天后肌电改变的起始与肠道形态、MMC数量及MMC分泌活性的变化。从小肠（绦虫的正常栖息地）以及胃、结肠和膀胱获取绦虫感染大鼠和对照大鼠的组织。将组织固定并染色以识别MMC并进行形态学测量。用肥大细胞稳定剂酮替芬处理长期植入肠道电极的绦虫感染和未感染大鼠，并监测体内肌电活动。在绦虫感染大鼠中，感染后第20天整个小肠的外肌层以及感染后第26天的利伯库恩隐窝分别出现增厚或加深。肌层厚度增加是由于环行肌层和纵行肌层的平滑肌肥大。感染后第26天首次观察到黏膜肥大细胞增多，且仅发生在绦虫感染大鼠的回肠。用酮替芬对肥大细胞进行药理稳定化处理并不能阻止绦虫感染期间肠道肌电改变的发生。感染微小膜壳绦虫的大鼠与未感染对照大鼠的胃、结肠和膀胱MMC数量及组织尺寸没有差异。感染8天后肌电改变的起始先于平滑肌肥大和黏膜肥大细胞增多的发生，并且可能是其发生的一个促成因素。综上所述，我们的数据表明肥大细胞不是微小膜壳绦虫感染期间肠道肌电改变的起始因素，也不是维持这种改变的慢性刺激因素。
