Suzuki Tohru, Sasaki Takeshi, Takagi Hisayoshi, Sato Kohji, Ueda Keiji
Department of Infectious Diseases, Hamamatsu University School of Medicine, 1-20-1 Handayama, Higashi-ku, Hamamatsu, Shizuoka 431-3192, Japan.
Parasitol Res. 2008 Nov;103(6):1289-95. doi: 10.1007/s00436-008-1130-1. Epub 2008 Aug 3.
Helper T (Th2) cells type 2 have a central role in host protective responses to gastrointestinal nematode parasite, Trichinella spiralis infection, but the actual effector mechanisms involved in parasite expulsion are still uncertain. Recent evidences suggest that mast cell recruitment and activation may associate with parasite elimination from host intestines in mice. On the other hand, IgE production may induce defensive responses to primary infection with the helminth in rats. The differences of host effector mechanisms to the same experimental infections might disturb our understanding of the host protective mechanisms to gastrointestinal nematode parasite infection. In order to redefine these differences, we investigated in detail the relationship between intestinal immune responses and worm expulsion following T. spiralis infection among several rat strains including mutants. As a result, there were significant correlations of parasite expulsion with mast cell hyperplasia in addition to serum IgE level. Moreover, mast cell-deficient and dysfunction rats showed delayed worm elimination from their gut. Therefore, the present study suggests that mast cells should also be one of the prominent effector cells involved in T. spiralis parasite expulsion in rats as well as mice.
辅助性T（Th2）2型细胞在宿主对胃肠道线虫寄生虫旋毛虫感染的保护性反应中起核心作用，但参与寄生虫排出的实际效应机制仍不明确。最近的证据表明，肥大细胞的募集和激活可能与小鼠肠道内寄生虫的清除有关。另一方面，IgE的产生可能会诱导大鼠对该蠕虫初次感染产生防御反应。宿主对相同实验性感染的效应机制差异可能会干扰我们对宿主对胃肠道线虫寄生虫感染的保护机制的理解。为了重新界定这些差异，我们详细研究了包括突变体在内的几种大鼠品系感染旋毛虫后肠道免疫反应与蠕虫排出之间的关系。结果发现，除血清IgE水平外，寄生虫排出与肥大细胞增生之间存在显著相关性。此外，肥大细胞缺陷和功能障碍的大鼠肠道内蠕虫清除延迟。因此，本研究表明，肥大细胞也是参与大鼠以及小鼠旋毛虫排出的重要效应细胞之一。
