Malkwitz Irene, Berndt Angela, Daugschies Arwid, Bangoura Berit
Institute of Parasitology, Faculty of Veterinary Medicine, Leipzig University, An den Tierkliniken 35, 04103, Leipzig, Germany.
Institute of Molecular Pathogenesis, Friedrich-Loeffler-Institut, Federal Research Institute for Animal Health, Naumburger Str. 96A, 07743, Jena, Germany.
Exp Parasitol. 2018 Apr;187:22-29. doi: 10.1016/j.exppara.2018.03.003. Epub 2018 Mar 6.
Toxoplasma gondii is known to be able to infect any nucleated cell including immune cells like macrophages. In addition, it is assumed that macrophages serve as trojan horse during distribution in hosts. The underlying causes of parasite host interaction remain yet not fully understood. The aim of the present study was to investigate susceptibility of chicken macrophages to infection with T. gondii and the process of infection in avian cells in comparison to cells of mammalian origin. Primary avian blood monocyte-derived macrophages were infected with tachyzoites of type II (ME49) and III (NED) strains. Long term observations of parasite replication in primary macrophages were compared to data obtained in an avian macrophage cell line (HD11) and a standard cultivation mammalian cell line (VERO). Furthermore, we assessed the immune response of the primary macrophages by long-term investigation of gene expression of IL-1 beta, IL-12p40, Lipopolysaccharide induced TNF-alpha factor (LITAF) and inducible nitric oxide synthase (iNOS) comparing viable and heat-inactivated tachyzoites of the ME49 strain. Albeit, we found no differences between both strains, replication of tachyzoites in avian primary macrophages was significantly different from immortalized cell lines HD11 and VERO. The crucial period of parasite replication was between 8 and 24 h post-infection coinciding with the upregulation of gene expression of cytokines and iNOS revealing an active macrophage response at this period. Gene expression in macrophages was higher after infection with viable tachyzoites than by exposure of cells to heat-inactivated tachyzoites. Hence, we conclude that the process of penetration is pivotal for host cell response to the parasite both in avian as in mammalian cells.
已知弓形虫能够感染任何有核细胞，包括巨噬细胞等免疫细胞。此外，据推测巨噬细胞在宿主体内传播过程中充当特洛伊木马。寄生虫与宿主相互作用的潜在原因仍未完全了解。本研究的目的是调查鸡巨噬细胞对弓形虫感染的易感性以及与哺乳动物来源的细胞相比，弓形虫在禽类细胞中的感染过程。用II型（ME49）和III型（NED）菌株的速殖子感染原代禽血单核细胞衍生的巨噬细胞。将原代巨噬细胞中寄生虫复制的长期观察结果与在禽巨噬细胞系（HD11）和标准培养哺乳动物细胞系（VERO）中获得的数据进行比较。此外，我们通过长期研究IL-1β、IL-12p40、脂多糖诱导的TNF-α因子（LITAF）和诱导型一氧化氮合酶（iNOS）的基因表达，比较ME49株活的和热灭活的速殖子，评估原代巨噬细胞的免疫反应。尽管我们发现两种菌株之间没有差异，但速殖子在禽原代巨噬细胞中的复制与永生化细胞系HD11和VERO显著不同。寄生虫复制的关键时期是感染后8至24小时，这与细胞因子和iNOS基因表达的上调相吻合，表明在此期间巨噬细胞有活跃反应。巨噬细胞在感染活的速殖子后的基因表达高于将细胞暴露于热灭活的速殖子后的基因表达。因此，我们得出结论，无论是在禽类细胞还是在哺乳动物细胞中，穿透过程对于宿主细胞对寄生虫的反应都至关重要。
