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刚地弓形虫的热休克蛋白90对宿主细胞入侵和速殖子生长至关重要。

The heat shock protein 90 of Toxoplasma gondii is essential for invasion of host cells and tachyzoite growth.

作者信息

Sun Hongchao, Zhuo Xunhui, Zhao Xianfeng, Yang Yi, Chen Xueqiu, Yao Chaoqun, Du Aifang

机构信息

Institute of Preventive Veterinary Medicine & Zhejiang Provincial Key Laboratory of Preventive Veterinary Medicine, College of Animal Sciences, Zhejiang Provincial Key Laboratory of Preventive Veterinary Medicine, Zhejiang University, Hangzhou 310058, PR China.

Shenzhen Entry-exit Inspection and Quarantine Bureau, Shenzhen 518045, PR China.

出版信息

Parasite. 2017;24:22. doi: 10.1051/parasite/2017023. Epub 2017 Jun 19.

DOI:10.1051/parasite/2017023
PMID:28627357
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5479401/
Abstract

Toxoplasma gondii is an obligate intracellular apicomplexan parasite that infects almost all warm-blooded vertebrates. Heat shock proteins (HSP) regulate key signal transduction events in many organisms, and heat shock protein 90 (Hsp90) plays an important role in growth, development, and virulence in several parasitic protozoa. Here, we discovered increased transcription of the Hsp90 gene under conditions for bradyzoite differentiation, i.e. alkaline and heat shock conditions in vitro, suggesting that Hsp90 may be connected with bradyzoite development in T. gondii. A knockout of the TgHsp90 strain (ΔHsp90) and a complementation strain were constructed. The TgHsp90 knockout cells were found to be defective in host-cell invasion, were not able to proliferate in vitro in Vero cells, and did not show long-time survival in mice in vivo. These inabilities of the knockout parasites were restored upon complementation of TgHsp90. These data unequivocally show that TgHsp90 contributes to bradyzoite development, and to invasion and replication of T. gondii in host cells.

摘要

刚地弓形虫是一种专性细胞内顶复门寄生虫，可感染几乎所有温血脊椎动物。热休克蛋白（HSP）在许多生物体中调节关键信号转导事件，热休克蛋白90（Hsp90）在几种寄生原生动物的生长、发育和毒力中发挥重要作用。在此，我们发现在体外缓殖子分化条件下，即碱性和热休克条件下，Hsp90基因的转录增加，这表明Hsp90可能与刚地弓形虫的缓殖子发育有关。构建了TgHsp90基因敲除株（ΔHsp90）和互补株。发现TgHsp90基因敲除细胞在宿主细胞侵袭方面存在缺陷，无法在体外Vero细胞中增殖，并且在体内小鼠中不能长期存活。在TgHsp90互补后，敲除寄生虫的这些无能表现得以恢复。这些数据明确表明，TgHsp90有助于缓殖子发育以及刚地弓形虫在宿主细胞中的侵袭和复制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60c1/5479401/cc35e47b8aff/parasite-24-22-fig8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60c1/5479401/ca2615de7c1f/parasite-24-22-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60c1/5479401/cc0804a98b68/parasite-24-22-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60c1/5479401/84310770ae9c/parasite-24-22-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60c1/5479401/fadd7fa2062a/parasite-24-22-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60c1/5479401/749a0a4e366e/parasite-24-22-fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60c1/5479401/f74711be7d5b/parasite-24-22-fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60c1/5479401/c0c215f436cf/parasite-24-22-fig7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60c1/5479401/cc35e47b8aff/parasite-24-22-fig8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60c1/5479401/ca2615de7c1f/parasite-24-22-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60c1/5479401/cc0804a98b68/parasite-24-22-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60c1/5479401/84310770ae9c/parasite-24-22-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60c1/5479401/fadd7fa2062a/parasite-24-22-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60c1/5479401/749a0a4e366e/parasite-24-22-fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60c1/5479401/f74711be7d5b/parasite-24-22-fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60c1/5479401/c0c215f436cf/parasite-24-22-fig7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60c1/5479401/cc35e47b8aff/parasite-24-22-fig8.jpg

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