Khan W I
Intestinal Disease Research Program, Department of Medicine, McMaster University, Hamilton, Ontario, Canada.
Parasitology. 2008 May;135(6):671-82. doi: 10.1017/S0031182008004381.
Infection and inflammation in the gastrointestinal (GI) tract induces a number of changes in the GI physiology of the host. Experimental infections with parasites represent valuable models to study the structural and physiological changes in the GI tract. This review addresses research on the interface between the immune system and GI physiology, dealing specifically with 2 major components of intestinal physiology, namely mucin production and muscle function in relation to host defence, primarily based on studies using the mouse-Trichinella spiralis system. These studies demonstrate that the infection-induced T helper 2 type immune response is critical in generating the alterations of infection-induced mucin production and muscle function, and that this immune-mediated alteration in gut physiology is associated with host defence mechanisms. In addition, by manipulating the host immune response, it is possible to modulate the accompanying physiological changes, which may have clinical relevance. In addition to enhancing our understanding of immunological control of GI physiological changes in the context of host defence against enteric infections, the data acquired using the mouse-T. spiralis model provide a basis for understanding the pathophysiology of a wide range of GI disorders associated with altered gut physiology.
胃肠道(GI)的感染与炎症会引起宿主胃肠道生理的一系列变化。寄生虫的实验性感染是研究胃肠道结构和生理变化的宝贵模型。本综述探讨了免疫系统与胃肠道生理学之间界面的研究,特别涉及肠道生理学的两个主要组成部分,即粘蛋白产生和与宿主防御相关的肌肉功能,主要基于使用小鼠-旋毛虫系统的研究。这些研究表明,感染诱导的2型辅助性T细胞免疫反应对于产生感染诱导的粘蛋白产生和肌肉功能改变至关重要,并且这种肠道生理学的免疫介导改变与宿主防御机制相关。此外,通过操纵宿主免疫反应,可以调节伴随的生理变化,这可能具有临床相关性。除了增强我们对宿主防御肠道感染背景下胃肠道生理变化的免疫控制的理解之外,使用小鼠-旋毛虫模型获得的数据为理解与肠道生理改变相关的广泛胃肠道疾病的病理生理学提供了基础。