Department of Biology, South Texas Center for Emerging Infectious Diseases, The University of Texas at San Antonio, One UTSA Circle, San Antonio, Texas 78249-1644, USA.
Parasitology. 2010 Mar;137(3):359-72. doi: 10.1017/S0031182009991971. Epub 2010 Jan 29.
Neurocysticercosis (NCC) is the most common parasitic disease of the central nervous system (CNS) caused by the larval form of the tapeworm Taenia solium. NCC has a long asymptomatic period with little or no inflammation, and the sequential progression to symptomatic NCC depends upon the intense inflammation associated with degeneration of larvae. The mechanisms involved in these progressive events are difficult to study in human patients. Thus it was necessary to develop an experimental model that replicated NCC. In this review, we describe studies of a murine model of NCC in terms of the release/secretion of parasite antigens, immune responses elicited within the CNS environment and subsequent pathogenesis. In particular, the kinetics of leukocyte subsets infiltrating into the brain are discussed in the context of disruption of the CNS barriers at distinct anatomical sites and the mechanisms contributing to these processes. In addition, production of various inflammatory mediators and the mechanisms involved in their induction by the Toll-like receptor signaling pathway are described. Overall, the knowledge gained from the mouse model of NCC has provided new insights for understanding the kinetics of events contributing to different stages of NCC and should aid in the formulation of more effective therapeutic approaches.
神经囊尾蚴病(NCC)是由绦虫猪带绦虫的幼虫引起的中枢神经系统(CNS)最常见的寄生虫病。NCC 有很长的无症状期,炎症很少或没有,而向有症状的 NCC 的序贯进展取决于与幼虫退化相关的强烈炎症。这些进行性事件中涉及的机制很难在人类患者中进行研究。因此,有必要开发一种可复制 NCC 的实验模型。在这篇综述中,我们根据寄生虫抗原的释放/分泌、在 CNS 环境中引发的免疫反应以及随后的发病机制,描述了 NCC 小鼠模型的研究。特别是,讨论了白细胞亚群在不同解剖部位的 CNS 屏障破坏时浸润大脑的动力学以及对这些过程有贡献的机制。此外,还描述了各种炎症介质的产生以及 Toll 样受体信号通路诱导它们的机制。总的来说,从 NCC 小鼠模型中获得的知识为理解导致 NCC 不同阶段的事件动力学提供了新的见解,并有助于制定更有效的治疗方法。