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双RNA测序显示,球虫寄生虫镰状艾美耳球虫对宿主免疫防御没有可塑性转录反应。

Dual RNA-seq reveals no plastic transcriptional response of the coccidian parasite Eimeria falciformis to host immune defenses.

作者信息

Ehret Totta, Spork Simone, Dieterich Christoph, Lucius Richard, Heitlinger Emanuel

机构信息

Institute of Biology, Molecular Parasitology, Humboldt-Universität zu Berlin, Philippstr. 13, Haus 14, 10115, Berlin, Germany.

FG16 - Mycotic and parasitic agents and mycobacteria, Robert Koch Institute, Berlin, Germany.

出版信息

BMC Genomics. 2017 Sep 5;18(1):686. doi: 10.1186/s12864-017-4095-6.

DOI:10.1186/s12864-017-4095-6
PMID:28870168
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5584376/
Abstract

BACKGROUND

Parasites can either respond to differences in immune defenses that exist between individual hosts plastically or, alternatively, follow a genetically canalized ("hard wired") program of infection. Assuming that large-scale functional plasticity would be discernible in the parasite transcriptome we have performed a dual RNA-seq study of the lifecycle of Eimeria falciformis using infected mice with different immune status as models for coccidian infections.

RESULTS

We compared parasite and host transcriptomes (dual transcriptome) between naïve and challenge infected mice, as well as between immune competent and immune deficient ones. Mice with different immune competence show transcriptional differences as well as differences in parasite reproduction (oocyst shedding). Broad gene categories represented by differently abundant host genes indicate enrichments for immune reaction and tissue repair functions. More specifically, TGF-beta, EGF, TNF and IL-1 and IL-6 are examples of functional annotations represented differently depending on host immune status. Much in contrast, parasite transcriptomes were neither different between Coccidia isolated from immune competent and immune deficient mice, nor between those harvested from naïve and challenge infected mice. Instead, parasite transcriptomes have distinct profiles early and late in infection, characterized largely by biosynthesis or motility associated functional gene groups, respectively. Extracellular sporozoite and oocyst stages showed distinct transcriptional profiles and sporozoite transcriptomes were found enriched for species specific genes and likely pathogenicity factors.

CONCLUSION

We propose that the niche and host-specific parasite E. falciformis uses a genetically canalized program of infection. This program is likely fixed in an evolutionary process rather than employing phenotypic plasticity to interact with its host. This in turn might limit the potential of the parasite to adapt to new host species or niches, forcing it to coevolve with its host.

摘要

背景

寄生虫对个体宿主间存在的免疫防御差异可能会产生可塑性反应,或者遵循一种基因固定(“硬连线”)的感染程序。假设在寄生虫转录组中可辨别出大规模的功能可塑性,我们以具有不同免疫状态的感染小鼠作为球虫感染模型,对镰形艾美耳球虫的生命周期进行了双RNA测序研究。

结果

我们比较了未感染和再次感染小鼠之间以及免疫健全和免疫缺陷小鼠之间的寄生虫和宿主转录组(双转录组)。具有不同免疫能力的小鼠表现出转录差异以及寄生虫繁殖(卵囊排出)的差异。宿主基因丰度不同所代表的广泛基因类别表明免疫反应和组织修复功能得到富集。更具体地说,TGF-β、EGF、TNF以及IL-1和IL-6是根据宿主免疫状态而表现不同的功能注释示例。相比之下,从免疫健全和免疫缺陷小鼠中分离出的球虫之间,以及从未感染和再次感染小鼠中收获的球虫之间,寄生虫转录组均无差异。相反,寄生虫转录组在感染早期和晚期具有不同的特征,分别主要由生物合成或运动相关的功能基因组所表征。细胞外子孢子和卵囊阶段表现出不同的转录特征,并且发现子孢子转录组富含物种特异性基因和可能的致病因子。

结论

我们提出,特定生态位和宿主的寄生虫镰形艾美耳球虫采用基因固定的感染程序。该程序可能在进化过程中固定下来,而不是利用表型可塑性与宿主相互作用。这反过来可能会限制寄生虫适应新宿主物种或生态位的潜力,迫使其与宿主共同进化。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b1b/5584376/e551648ee9ad/12864_2017_4095_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b1b/5584376/65d03bdcca7e/12864_2017_4095_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b1b/5584376/8a193bea45cb/12864_2017_4095_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b1b/5584376/d3e19e29a9e9/12864_2017_4095_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b1b/5584376/e551648ee9ad/12864_2017_4095_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b1b/5584376/65d03bdcca7e/12864_2017_4095_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b1b/5584376/8a193bea45cb/12864_2017_4095_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b1b/5584376/d3e19e29a9e9/12864_2017_4095_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b1b/5584376/e551648ee9ad/12864_2017_4095_Fig4_HTML.jpg

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