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同域与异域进化环境塑造了生物型/血吸虫相互作用中的差异免疫反应。

Sympatric versus allopatric evolutionary contexts shape differential immune response in Biomphalaria / Schistosoma interaction.

机构信息

Univ. Perpignan Via Domitia, Interactions Hôtes Pathogènes Environnements UMR 5244, CNRS, IFREMER, Univ. Montpellier, Perpignan, France.

School of Marine and Atmospheric Sciences, Stony Brook University, Stony Brook, New York, United States of America.

出版信息

PLoS Pathog. 2019 Mar 20;15(3):e1007647. doi: 10.1371/journal.ppat.1007647. eCollection 2019 Mar.

DOI:10.1371/journal.ppat.1007647
PMID:30893368
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6443186/
Abstract

Selective pressures between hosts and their parasites can result in reciprocal evolution or adaptation of specific life history traits. Local adaptation of resident hosts and parasites should lead to increase parasite infectivity/virulence (higher compatibility) when infecting hosts from the same location (in sympatry) than from a foreign location (in allopatry). Analysis of geographic variations in compatibility phenotypes is the most common proxy used to infer local adaptation. However, in some cases, allopatric host-parasite systems demonstrate similar or greater compatibility than in sympatry. In such cases, the potential for local adaptation remains unclear. Here, we study the interaction between Schistosoma and its vector snail Biomphalaria in which such discrepancy in local versus foreign compatibility phenotype has been reported. Herein, we aim at bridging this gap of knowledge by comparing life history traits (immune cellular response, host mortality, and parasite growth) and molecular responses in highly compatible sympatric and allopatric Schistosoma/Biomphalaria interactions originating from different geographic localities (Brazil, Venezuela and Burundi). We found that despite displaying similar prevalence phenotypes, sympatric schistosomes triggered a rapid immune suppression (dual-RNAseq analyses) in the snails within 24h post infection, whereas infection by allopatric schistosomes (regardless of the species) was associated with immune cell proliferation and triggered a non-specific generalized immune response after 96h. We observed that, sympatric schistosomes grow more rapidly. Finally, we identify miRNAs differentially expressed by Schistosoma mansoni that target host immune genes and could be responsible for hijacking the host immune response during the sympatric interaction. We show that despite having similar prevalence phenotypes, sympatric and allopatric snail-Schistosoma interactions displayed strong differences in their immunobiological molecular dialogue. Understanding the mechanisms allowing parasites to adapt rapidly and efficiently to new hosts is critical to control disease emergence and risks of Schistosomiasis outbreaks.

摘要

宿主和寄生虫之间的选择压力会导致特定生活史特征的相互进化或适应。当感染来自同一地点(同域)的宿主时,驻留宿主和寄生虫的本地适应应该会导致寄生虫感染性/毒力增加(更高的相容性),而不是来自外地的宿主(异域)。兼容性表型的地理变异分析是推断本地适应最常用的替代方法。然而,在某些情况下,异域宿主-寄生虫系统表现出与同域相似或更高的相容性。在这种情况下,本地适应的潜力仍不清楚。在这里,我们研究了血吸虫及其载体蜗牛 B. glabrata 之间的相互作用,在这种情况下,已经报道了本地与外地兼容性表型的差异。在这里,我们旨在通过比较来自不同地理区域(巴西、委内瑞拉和布隆迪)的高度相容的同域和异域血吸虫/蜗牛相互作用的生活史特征(免疫细胞反应、宿主死亡率和寄生虫生长)和分子反应来弥合这一知识差距。我们发现,尽管表现出相似的流行表型,但在感染后 24 小时内,同域血吸虫会迅速抑制蜗牛的免疫(双 RNA-seq 分析),而感染异域血吸虫(无论物种如何)与免疫细胞增殖有关,并在 96 小时后引发非特异性全身性免疫反应。我们观察到,同域血吸虫生长得更快。最后,我们确定了曼氏血吸虫中差异表达的 miRNA,这些 miRNA 靶向宿主免疫基因,可能是在同域相互作用中劫持宿主免疫反应的原因。我们表明,尽管具有相似的流行表型,但同域和异域蜗牛-血吸虫相互作用在其免疫生物学分子对话中表现出强烈的差异。了解寄生虫如何快速有效地适应新宿主的机制对于控制疾病的出现和血吸虫病爆发的风险至关重要。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92f3/6443186/cb805bef2ca4/ppat.1007647.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92f3/6443186/5d7852a15cfa/ppat.1007647.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92f3/6443186/2d9d3b4285c4/ppat.1007647.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92f3/6443186/e8738f3fb8f0/ppat.1007647.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92f3/6443186/0b6e0a13e77a/ppat.1007647.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92f3/6443186/f87c559dbd44/ppat.1007647.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92f3/6443186/000c24bc1f46/ppat.1007647.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92f3/6443186/cb805bef2ca4/ppat.1007647.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92f3/6443186/5d7852a15cfa/ppat.1007647.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92f3/6443186/2d9d3b4285c4/ppat.1007647.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92f3/6443186/e8738f3fb8f0/ppat.1007647.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92f3/6443186/0b6e0a13e77a/ppat.1007647.g004.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92f3/6443186/000c24bc1f46/ppat.1007647.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92f3/6443186/cb805bef2ca4/ppat.1007647.g007.jpg

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