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通过添加海洋硅藻中的β-葡聚糖增强凡纳滨对虾的免疫力。

Enhancing Pacific white shrimp immunity against through β-glucan supplementation from marine diatoms.

作者信息

Pooljun Chettupon, Jariyapong Pitchanee, Laksana-Aut Patcharapon, Hirono Ikuo, Wuthisuthimethavee Suwit

机构信息

Akkhraratchakumari Veterinary College, Walailak University, Thasala, Nakhon Si Thammarat, 80160, Thailand.

Center of Excellence in Aquaculture Technology and Innovation, School of Agricultural Technology and Food Industry, Walailak University, Thasala District, Nakhon Si Thammarat, 80160, Thailand.

出版信息

Vet World. 2025 Apr;18(4):1047-1058. doi: 10.14202/vetworld.2025.1047-1058. Epub 2025 Apr 30.

DOI:10.14202/vetworld.2025.1047-1058
PMID:40453940
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12123291/
Abstract

BACKGROUND AND AIM

Pacific white shrimp () is a principal species in global aquaculture. However, outbreaks of , the etiological agent of acute hepatopancreatic necrosis disease (AHPND), cause substantial economic losses. β-glucans derived from marine diatoms, (CH) and (TH), have shown potential as immunostimulants to enhance shrimp resistance to pathogenic infections. This study aimed to evaluate the effects of β-glucans derived from CH, TH, and their combination on growth performance, immune responses, and survival of and to elucidate the underlying molecular mechanisms through transcriptomic and gene silencing approaches.

MATERIALS AND METHODS

Juvenile shrimp were assigned to four dietary groups for 30 days: Control (β-glucan-free), β-glucan from CH, TH, and a mixture of both (CH and TH) (CHTH). Growth performance, total hemocyte count (THC), and survival rate were evaluated. RNA-seq was performed on hepatopancreas samples after 14 days to identify differentially expressed genes (DEGs). Key immune-related DEGs were validated by quantitative reverse transcription polymerase chain reaction (qRT-PCR). Functional analysis of the () gene was conducted through RNA interference (RNAi), followed by challenge.

RESULTS

The CHTH diet group exhibited significantly enhanced growth metrics and the highest survival rate. Transcriptomic analysis revealed 1,902 DEGs in the CHTH group compared to control, with 915 upregulated and 987 downregulated genes. qRT-PCR validated the expression trends of selected immune-related genes, notably , which showed robust upregulation. RNAi-mediated knockdown reduced survival upon bacterial challenge, confirming its role in β-glucan-induced immunity.

CONCLUSION

β-glucans derived from CH and TH, particularly in combination, significantly enhance growth performance and immunocompetence in . These findings underscore the potential of marine diatom-derived β-glucans as viable immunostimulants to mitigate AHPND in shrimp aquaculture, offering a sustainable alternative to antibiotic use.

摘要

背景与目的

凡纳滨对虾(Litopenaeus vannamei)是全球水产养殖中的主要品种。然而,急性肝胰腺坏死病(AHPND)的病原体副溶血弧菌(Vibrio parahaemolyticus)的爆发造成了巨大的经济损失。来源于海洋硅藻三角褐指藻(Phaeodactylum tricornutum)(CH)和海链藻(Thalassiosira weissflogii)(TH)的β-葡聚糖已显示出作为免疫刺激剂增强对虾抵抗病原体感染的潜力。本研究旨在评估来源于CH、TH的β-葡聚糖及其组合对凡纳滨对虾生长性能、免疫反应和存活的影响,并通过转录组学和基因沉默方法阐明潜在的分子机制。

材料与方法

将幼虾分为四个日粮组,为期30天:对照组(不含β-葡聚糖)、来源于CH的β-葡聚糖组、来源于TH的β-葡聚糖组以及两者的混合物(CH和TH)(CHTH)组。评估生长性能、总血细胞计数(THC)和存活率。在14天后对肝胰腺样本进行RNA测序,以鉴定差异表达基因(DEG)。通过定量逆转录聚合酶链反应(qRT-PCR)验证关键免疫相关DEG。通过RNA干扰(RNAi)对Toll(Toll)基因进行功能分析,随后进行副溶血弧菌攻毒。

结果

CHTH日粮组的生长指标显著提高,存活率最高。转录组分析显示,与对照组相比,CHTH组有1902个DEG,其中915个基因上调,987个基因下调。qRT-PCR验证了所选免疫相关基因的表达趋势,尤其是Toll,其显示出强烈上调。RNAi介导的Toll基因敲低降低了细菌攻毒后的存活率,证实了其在β-葡聚糖诱导的免疫中的作用。

结论

来源于CH和TH的β-葡聚糖,特别是两者组合,显著提高了凡纳滨对虾的生长性能和免疫能力。这些发现强调了海洋硅藻来源的β-葡聚糖作为减轻对虾养殖中AHPND的可行免疫刺激剂的潜力,为抗生素使用提供了可持续的替代方案。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7dc8/12123291/b7cdbd3e97c8/Vetworld-18-1047-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7dc8/12123291/63b3e84293ef/Vetworld-18-1047-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7dc8/12123291/213a3328dd4d/Vetworld-18-1047-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7dc8/12123291/b2da8bcbd473/Vetworld-18-1047-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7dc8/12123291/a12386ea2cf4/Vetworld-18-1047-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7dc8/12123291/9692d9f39508/Vetworld-18-1047-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7dc8/12123291/b7cdbd3e97c8/Vetworld-18-1047-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7dc8/12123291/63b3e84293ef/Vetworld-18-1047-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7dc8/12123291/213a3328dd4d/Vetworld-18-1047-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7dc8/12123291/b2da8bcbd473/Vetworld-18-1047-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7dc8/12123291/a12386ea2cf4/Vetworld-18-1047-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7dc8/12123291/9692d9f39508/Vetworld-18-1047-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7dc8/12123291/b7cdbd3e97c8/Vetworld-18-1047-g006.jpg

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