Ojcius D M, Perfettini J L, Bonnin A, Laurent F
Unité de biologie des interactions cellulaires, CNRS URA 1960, Institut Pasteur, Paris, France.
Microbes Infect. 1999 Dec;1(14):1163-8. doi: 10.1016/s1286-4579(99)00246-4.
The protozoan parasite Cryptosporidium parvum causes persistent diarrhea and malnutrition in children and the diarrhea-wasting syndrome in AIDS. No therapy exists for eliminating the parasite in the absence of a healthy immune response. Although it had been reported that infection of intestinal cell lines with C. parvum leads to host cell death, the mechanisms of cytolysis have not been characterized. We show here that infection with C. parvum leads to typical apoptotic nuclear condensation and DNA fragmentation in host cells. Both nuclear condensation and DNA fragmentation are inhibited by a caspase inhibitor, showing that caspases are involved in this type of apoptosis. Finally, blocking apoptosis with the caspase inhibitor increases the percentage of infected cells, suggesting that parasites may use apoptosis to exit from the infected cell or that the infected cells may eliminate the parasite through apoptosis. These results suggest that apoptosis could be involved in the pathogenesis of C. parvum infections in vivo, and raise the possibility that therapeutic interference with host cell death could alter the course of the pathology in vivo.
原生动物寄生虫微小隐孢子虫可导致儿童持续性腹泻和营养不良以及艾滋病患者的腹泻消耗综合征。在缺乏健康免疫反应的情况下,不存在消除该寄生虫的疗法。尽管有报道称微小隐孢子虫感染肠道细胞系会导致宿主细胞死亡,但细胞溶解机制尚未明确。我们在此表明,微小隐孢子虫感染会导致宿主细胞出现典型的凋亡性核浓缩和DNA片段化。核浓缩和DNA片段化均被半胱天冬酶抑制剂抑制,表明半胱天冬酶参与了这种类型的凋亡。最后,用半胱天冬酶抑制剂阻断凋亡会增加被感染细胞的百分比,这表明寄生虫可能利用凋亡从被感染细胞中逸出,或者被感染细胞可能通过凋亡清除寄生虫。这些结果表明凋亡可能参与了微小隐孢子虫体内感染的发病机制,并增加了对宿主细胞死亡进行治疗性干预可能改变体内病理过程的可能性。