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对鮰爱德华氏菌与青石斑鱼相互作用的代谢组学研究。

Metabolomics insights into the interaction between Pseudomonas plecoglossicida and Epinephelus coioides.

机构信息

College of Ocean Food and Biological Engineering, Jimei University, Xiamen, 361021, China.

Xiamen Key Laboratory of Marine Functional Food, Xiamen, 361021, China.

出版信息

Sci Rep. 2022 Aug 3;12(1):13309. doi: 10.1038/s41598-022-17387-6.

DOI:10.1038/s41598-022-17387-6
PMID:35922642
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9349296/
Abstract

As a highly infectious epidemic in aquaculture, Pseudomonas plecoglossicida infection results in high mortality of teleosts and serious economic losses. Host-pathogen interactions shape the outcome of an infection, yet we still understand little about the molecular mechanism of these pathogen-mediated processes. Here, a P. plecoglossicida strain (NZBD9) and Epinephelus coioides were investigated as a model system to characterize pathogen-induced host metabolic remodeling over the course of infection. We present a non-targeted metabolomics profiling of E. coioides spleens from uninfected E. coioides and those infected with wild-type and clpV-RNA interference (RNAi) strains. The most significant changes of E. coioides upon infection were associated with amino acids, lysophospatidylcholines, and unsaturated fatty acids, involving disturbances in host nutritional utilization and immune responses. Dihydrosphingosine and fatty acid 16:2 were screened as potential biomarkers for assessing P. plecoglossicida infection. The silencing of the P. plecoglossicida clpV gene significantly recovered the lipid metabolism of infected E. coioides. This comprehensive metabolomics study provides novel insights into how P. plecoglossicida shape host metabolism to support their survival and replication and highlights the potential of the virulence gene clpV in the treatment of P. plecoglossicida infection in aquaculture.

摘要

作为水产养殖中一种高度传染性的流行病,鮰爱德华氏菌感染会导致硬骨鱼类的高死亡率和严重的经济损失。宿主-病原体相互作用决定了感染的结果,但我们对这些病原体介导的过程的分子机制仍知之甚少。在这里,我们以鮰鱼为模型系统,研究了一株鮰爱德华氏菌(NZBD9)和斜带石斑鱼,以阐明病原菌诱导的宿主代谢重编程过程。我们对未感染斜带石斑鱼和感染野生型及 clpV-RNA 干扰(RNAi)菌株的斜带石斑鱼脾脏进行了非靶向代谢组学分析。感染后斜带石斑鱼发生的最显著变化与氨基酸、溶血磷脂酰胆碱和不饱和脂肪酸有关,涉及到宿主营养利用和免疫反应的紊乱。二氢神经鞘氨醇和脂肪酸 16:2 被筛选为评估鮰爱德华氏菌感染的潜在生物标志物。沉默鮰爱德华氏菌的 clpV 基因可显著恢复感染斜带石斑鱼的脂质代谢。这项全面的代谢组学研究为我们深入了解鮰爱德华氏菌如何塑造宿主代谢以支持其存活和复制提供了新的见解,并强调了毒力基因 clpV 在水产养殖中治疗鮰爱德华氏菌感染的潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7663/9349296/d4642872bc86/41598_2022_17387_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7663/9349296/401ee50d1023/41598_2022_17387_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7663/9349296/d854d54ae4a7/41598_2022_17387_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7663/9349296/cf8901713df7/41598_2022_17387_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7663/9349296/4689af2bd216/41598_2022_17387_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7663/9349296/01a787f22548/41598_2022_17387_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7663/9349296/d4642872bc86/41598_2022_17387_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7663/9349296/401ee50d1023/41598_2022_17387_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7663/9349296/d854d54ae4a7/41598_2022_17387_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7663/9349296/cf8901713df7/41598_2022_17387_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7663/9349296/4689af2bd216/41598_2022_17387_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7663/9349296/01a787f22548/41598_2022_17387_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7663/9349296/d4642872bc86/41598_2022_17387_Fig6_HTML.jpg

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