Chen Ke-Min, Lee Hsiu-Hsiung, Lu Kuang-Hui, Tseng Yu-Kai, Hsu Li-Sung, Chou Hui-Lin, Lai Shih-Chan
Department of Parasitology, Chung Shan Medical University, 110, Section 1, Chien-Kuo North Road, Taichung 402, Taiwan, ROC.
Int J Parasitol. 2004 Sep;34(10):1147-56. doi: 10.1016/j.ijpara.2004.07.004.
Angiostrongylosis is a neurological disorder caused by invasion of the central nervous system by developing larvae of Angiostrongylus cantonensis. Purkinje cells in infected mouse cerebellums are small and irregular with degenerative atrophy or partial loss. Ultrastructural changes in degenerative cells included enlarged vacuolar structures and swollen mitochondria within the cytoplasm. The matrix metalloproteinase-9 mRNA which is low in normal cerebellums was expressed in A. cantonensis-infected mice cerebellum prior to Purkinje cell degeneration. Matrix metalloproteinase-9 protein level and enzyme activity increased when the Purkinje cells appeared degenerated. Using immunohistochemistry, matrix metalloproteinase-9 was localised within degenerative Purkinje cells. In addition, when the specific matrix metalloproteinase inhibitor, GM6001, was added, matrix metalloproteinase-9 enzyme activity was reduced by 41.6%. The numbers of degenerative Purkinje cells increased significantly upon establishment of infection but subsided upon inhibition. These results suggested that the expression of matrix metalloproteinase-9 may be associated with degeneration of Purkinje cells in mouse cerebellum infected by A. cantonensis.
广州管圆线虫病是一种由广州管圆线虫发育中的幼虫侵入中枢神经系统引起的神经疾病。感染小鼠小脑的浦肯野细胞小且不规则，伴有退行性萎缩或部分缺失。退行性细胞的超微结构变化包括细胞质内空泡结构增大和线粒体肿胀。正常小脑中含量较低的基质金属蛋白酶-9 mRNA在广州管圆线虫感染的小鼠小脑浦肯野细胞退化之前就已表达。当浦肯野细胞出现退化时，基质金属蛋白酶-9的蛋白水平和酶活性增加。通过免疫组织化学方法，基质金属蛋白酶-9定位于退化的浦肯野细胞内。此外，当加入特异性基质金属蛋白酶抑制剂GM6001时，基质金属蛋白酶-9的酶活性降低了41.6%。感染确立后，退化的浦肯野细胞数量显著增加，但在受到抑制后减少。这些结果表明，基质金属蛋白酶-9的表达可能与广州管圆线虫感染的小鼠小脑中浦肯野细胞的退化有关。
