Trichinella inflammatory myopathy: host or parasite strategy?

Trichinella inflammatory myopathy: host or parasite strategy?
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DOI:
10.1186/1756-3305-4-42
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发表时间:
2011-03-23
影响因子:
3.2
通讯作者:
Chiumiento L
Chiumiento L
中科院分区:
医学2区
文献类型:
--
作者:
Bruschi F;Chiumiento L

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旋毛虫寄生线虫与肌肉有着特殊的关系,由于其独特的细胞内定位于骨骼肌细胞,在形态学和生物化学上完全致力于成为寄生虫的保护生态位,也被称为看护细胞。旋毛虫的长期肌肉感染表现出与宿主免疫反应的强烈相互作用,主要表现为Th2表型。本综述的目的是阐明在不同的实验模型中,如敲除或免疫调节小鼠,Th2宿主免疫反应在旋毛虫病期间在肌肉水平的作用。特别是,在敲除小鼠中,IL-10在调节炎症强度方面的关键作用是显而易见的。肌肉宿主对旋毛虫的免疫反应部分受到寄生虫肠道期的调节,与同步注射新生幼虫感染的动物相比,肠道期强调了随后肌肉炎症的强度。在嗜酸性粒细胞消融的小鼠(如PHIL和GATA-动物)中,观察到巨噬细胞中NOS2表达增加,这是由IFN-γ释放增加驱动的,从而导致肌肉幼虫损伤。此外,利用重组IL-12调节感染的肠道阶段,增加肌肉寄生虫负担,延缓成虫从肠道排出。此外,在旋毛虫病的肠道期给予一种细菌来源的Th1佐剂,称为幽门螺杆菌中性粒细胞激活蛋白(HP-NAP),在肌肉水平上改变Th2依赖性反应。所有这些来自文献的数据都描述了寄生虫和宿主免疫反应之间的相互适应,以实现两种进化力量之间的战略妥协,从而指向两个物种的生存。
The parasitic nematode Trichinella has a special relation with muscle, because of its unique intracellular localization in the skeletal muscle cell, completely devoted in morphology and biochemistry to become the parasite protective niche, otherwise called the nurse cell. The long-lasting muscle infection of Trichinella exhibits a strong interplay with the host immune response, mainly characterized by a Th2 phenotype. The aim of this review is to illustrate the role of the Th2 host immune response at the muscle level during trichinellosis in different experimental models, such as knock-out or immuno-modulated mice. In particular, in knock-out mice a crucial role of IL-10 is evident for the regulation of inflammation intensity. The muscular host immune response to Trichinella is partially regulated by the intestinal phase of the parasite which emphasizes the intensity of the following muscle inflammation compared with animals infected by synchronized injections of newborn larvae. In eosinophil-ablated mice such as PHIL and GATA-- animals it was observed that there was an increased NOS2 expression in macrophages, driven by higher IFN-γ release, thus responsible for muscle larva damage. Besides modulation of the intestinal stage of the infection, using recombinant IL-12, increases the muscular parasite burden delaying adult worm expulsion from the intestine. Furthermore, a Th1 adjuvant of bacterial origin called Helicobacter pylori neutrophil activating protein (HP-NAP), administered during the intestinal phase of trichinellosis, alters the Th2 dependent response at muscle level. All these data from the literature delineate then a mutual adaptation between parasite and host immune response in order to achieve a strategic compromise between two evolutionary forces pointed towards the survival of both species.
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发表时间: 2006-09-01
影响因子: 2.2
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