Specific Strains of Honeybee Gut Lactobacillus Stimulate Host Immune System to Protect against Pathogenic Hafnia alvei.

Specific Strains of Honeybee Gut Lactobacillus Stimulate Host Immune System to Protect against Pathogenic Hafnia alvei.
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蜜蜂肠道乳酸菌的特定菌株刺激宿主免疫系统以预防致病性蜂巢哈夫尼亚

DOI:
10.1128/spectrum.01896-21
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发表时间:
2022-02-23
影响因子:
3.7
通讯作者:
Zheng H
Zheng H
中科院分区:
生物学1区
文献类型:
--
作者:
Lang H;Duan H;Wang J;Zhang W;Guo J;Zhang X;Hu X;Zheng H

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蜜蜂肠道微生物区系在宿主生理和代谢中起着重要作用。近年来的研究表明,蜜蜂体内的微生物对蜜蜂免疫系统的调节有着重要的作用,对病原菌粘质沙雷氏菌(Serratia marcescens)具有保护作用。然而,只有少数的核心肠道成员在免疫功能的调节进行了研究。在这里,我们探讨了不同的蜜蜂肠道细菌物种如何帮助清除致病性蜂房哈夫尼菌,这种菌会导致蜜蜂败血症,死亡率很高。我们发现,蜜蜂吉利杆菌W8136和蜜蜂乳杆菌W8172都能保护蜜蜂免受条件致病菌的侵害,而来自吉利杆菌和乳杆菌的另外两种菌株则不影响H.肺泡。转录组学分析表明,肠道物种诱导不同的表达谱在肠道。具体来说,来自Toll途径的两个调节基因,识别革兰氏阳性菌的PGRP-S3和与Toll蛋白结合以进行下游信号传导的Spätzle,被L. apis。相应地,多个编码抗菌蛋白的基因也被L. apis。有趣的是,我们发现apidaecin的表达增加,这也表现出高的体外抑制作用,H。肺泡。为了阐明不同菌株在宿主免疫调节中的差异,比较基因组分析表明,L.蜜蜂可能参与蜜蜂Toll信号传导和抗菌蛋白产生的激活。蜜蜂是支持全球农业经济和粮食供应的重要授粉者。最近蜜蜂数量的下降与几个因素有关,而病原体感染被认为是最重要的因素之一。虽然已经确定了有限数量的细菌病原体,但蜂房哈夫尼菌是引起成年蜜蜂败血症的病原体之一。在本研究中,我们发现两种蜜蜂肠道成员,吉尔氏杆菌和乳酸杆菌可以清除H。从入侵。特异性菌株的单菌落定殖可以刺激宿主Toll信号通路和AMP的下游表达。具体而言,由肠道共生体上调的阿皮达星对病原体更有效。此外,我们的基因组分析表明,乳酸杆菌菌株特异性的表面层蛋白是Toll信号传导的重要驱动因素,突出了蜜蜂肠道菌株在调节宿主免疫系统方面的变化。
Honeybee gut microbiota plays an important role in host physiology and metabolism. Recent studies have shown that the influence of the resident microorganisms in the regulation of honeybee immune system is profound, which protects against the pathogen Serratia marcescens. However, only few of the core gut members in the regulation of immune functions have been studied. Here, we explored how different bee gut bacterial species aided in the clearance of the pathogenic Hafnia alvei, which causes bee septicemia with a high mortality rate. We found that both Gilliamella apicola W8136 and Lactobacillus apis W8172 protect honeybees from the opportunistic pathogen, while two other strains from Gilliamella and Lactobacillus did not affect the invasion of H. alvei. Transcriptomic analysis revealed that gut species induced different expression profiles in the gut. Specifically, two regulator genes from the Toll pathway, PGRP-S3 recognizing Gram-positive and Spätzle that bind to the Toll protein for the downstream signal transduction, were elevated by L. apis. Correspondingly, multiple genes encoding antibacterial proteins were also stimulated by L. apis. Interestingly, we found an increased expression of apidaecin, which also exhibited a high in vitro inhibitory effect on H. alvei. To elucidate the difference of strains in the host’s immune regulation, comparative genomic analyses indicate that the S-layer proteins unique to L. apis are potentially involved in honeybee Toll signaling and the activation of antibacterial protein production. IMPORTANCE Honeybees are essential pollinators supporting global agricultural economies and food supplies. Recent honeybee decline has been linked to several factors, while pathogen infection is considered one of the most significant contributing factors. Although a limited number of bacterial pathogens have been identified, Hafnia alvei is one of the pathogens causing septicemia in adult bees. In this study, we showed that two bee gut members, Gilliamella and Lactobacillus, can clear H. alvei from invasion. Mono-colonization of specific strains can stimulate the host Toll signaling pathway and the downstream expression of AMPs. Specifically, apidaecin upregulated by the gut symbionts is more effective against the pathogen. Moreover, our genomic analysis suggests that the surface-layer proteins specific to Lactobacillus strains are an important driver of Toll signaling, highlighting the variation of bee gut strains in regulating the host immune system.
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