PDF(Pubmed)
Abstract：
Angiostrongylus cantonensis, a zoonotic parasite, can invade the human central nervous system (CNS) and cause acute eosinophilic meningitis or eosinophilic meningoencephalitis. Mice infected with A. cantonensis show elevated levels of pro-inflammatory cytokines, plasminogen activators, and matrix metalloproteinase-9, resulting in disruption of the blood-brain barrier (BBB) and immune cell infiltration into the CNS. Caveolin-1 (Cav-1) regulates the permeability of the BBB, which affects immune cells and cerebrospinal fluid. This intricate interaction ultimately fuels the progression of brain damage and edema. This study aims to investigate the regulatory role of Cav-1 in the pathogenesis of meningoencephalitis induced by A. cantonensis infection. We investigated pathological alterations by triphenyl-tetrazolium chloride, brain water content, BBB permeability, Western blot analysis, and gelatin zymography in BALB/c mice after A. cantonensis. The study evaluates the critical role of Cav-1 regulation through the TLR4/MyD88 signaling pathway, modulates tight junction proteins, influences BBB permeability, and contributes to brain damage in A. cantonensis-induced meningoencephalitis.
摘要：
广州管圆线虫，一种人畜共患寄生虫,可以侵入人体中枢神经系统（CNS）并引起急性嗜酸性粒细胞性脑膜炎或嗜酸性粒细胞性脑膜脑炎。感染A.cantonensis的小鼠显示促炎细胞因子水平升高，纤溶酶原激活剂，和基质金属蛋白酶-9，导致血脑屏障（BBB）的破坏和免疫细胞渗入CNS。小窝蛋白-1（Cav-1）调节BBB的渗透性，影响免疫细胞和脑脊液。这种复杂的相互作用最终促进了脑损伤和水肿的进展。本研究旨在探讨Cav-1在A感染诱发脑膜脑炎发病机制中的调节作用。我们调查了三苯基-四唑氯化物的病理改变，脑含水量,BBB通透性,蛋白质印迹分析,和A.cantonensis后BALB/c小鼠的明胶酶谱。本研究通过TLR4/MyD88信号通路评估Cav-1调控的关键作用,调节紧密连接蛋白，影响BBB渗透率，并有助于A.cantonensis诱发的脑膜脑炎的脑损伤。
