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急性肝胰腺坏死病期间对虾胃部的代谢变化及牛磺胆酸盐的影响

Metabolic Alterations in Shrimp Stomach During Acute Hepatopancreatic Necrosis Disease and Effects of Taurocholate on .

作者信息

Kumar Ramya, Tung Teng-Chun, Ng Tze Hann, Chang Che-Chih, Chen Yi-Lun, Chen Yi-Min, Lin Shih-Shun, Wang Han-Ching

机构信息

Department of Biotechnology and Bioindustry Sciences, National Cheng Kung University, Tainan, Taiwan.

International Center for Scientific Development of Shrimp Aquaculture, National Cheng Kung University, Tainan, Taiwan.

出版信息

Front Microbiol. 2021 Apr 20;12:631468. doi: 10.3389/fmicb.2021.631468. eCollection 2021.

DOI:10.3389/fmicb.2021.631468
PMID:33959104
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8093816/
Abstract

Acute hepatopancreatic necrosis disease (AHPND), a recently emerged bacterial shrimp disease, has increased shrimp mortality and caused huge economic losses in many Asian countries. However, molecular factors underlying pathogenesis of this disease remain largely unknown. Our objective was to characterize metabolic alterations in shrimp stomach during AHPND and determine effects of taurocholate on AHPND-causing . Based on metabolomics, pathways for lipid metabolism and for primary bile acid (BA) synthesis were majorly affected following AHPND infection. Bile acid metabolites, namely taurocholate, were downregulated in the metabolomics database. This prompted us to study effects of taurocholate on biofilm formation, PirAB toxin release and biofilm detachment capabilities in AHPND-causing . Treatment of this bacterium with high concentration of taurocholate, a primary bile acid, induced biofilm formation, PirAB toxin release and facilitated the dispersion of bacterial cells. Taken together, our findings suggest that AHPND infection can affect the lipid metabolites in shrimp stomach, and further suggest that the primary bile acid taurocholate is important for the virulence of AHPND-causing .

摘要

急性肝胰腺坏死病(AHPND)是一种最近出现的对虾细菌性疾病,在许多亚洲国家导致了对虾死亡率上升并造成了巨大经济损失。然而,这种疾病发病机制的分子因素在很大程度上仍然未知。我们的目标是表征AHPND期间对虾胃部的代谢变化,并确定牛磺胆酸盐对引起AHPND的[细菌名称未给出]的影响。基于代谢组学,AHPND感染后脂质代谢途径和初级胆汁酸(BA)合成途径受到主要影响。胆汁酸代谢物,即牛磺胆酸盐,在代谢组学数据库中下调。这促使我们研究牛磺胆酸盐对引起AHPND的[细菌名称未给出]的生物膜形成、PirAB毒素释放和生物膜脱离能力的影响。用高浓度的初级胆汁酸牛磺胆酸盐处理这种细菌,诱导了生物膜形成、PirAB毒素释放并促进了细菌细胞的分散。综上所述,我们的研究结果表明AHPND感染会影响对虾胃部的脂质代谢物,并进一步表明初级胆汁酸牛磺胆酸盐对引起AHPND的[细菌名称未给出]的毒力很重要。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e207/8093816/cf37c5c7d354/fmicb-12-631468-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e207/8093816/8c105f9377ee/fmicb-12-631468-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e207/8093816/18e813cfc5a3/fmicb-12-631468-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e207/8093816/f7faa6cb976e/fmicb-12-631468-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e207/8093816/42b418ca4aac/fmicb-12-631468-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e207/8093816/b43f8a8501b3/fmicb-12-631468-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e207/8093816/7d5f05d5b137/fmicb-12-631468-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e207/8093816/82b2b693fe35/fmicb-12-631468-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e207/8093816/cf37c5c7d354/fmicb-12-631468-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e207/8093816/8c105f9377ee/fmicb-12-631468-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e207/8093816/18e813cfc5a3/fmicb-12-631468-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e207/8093816/f7faa6cb976e/fmicb-12-631468-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e207/8093816/42b418ca4aac/fmicb-12-631468-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e207/8093816/b43f8a8501b3/fmicb-12-631468-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e207/8093816/7d5f05d5b137/fmicb-12-631468-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e207/8093816/82b2b693fe35/fmicb-12-631468-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e207/8093816/cf37c5c7d354/fmicb-12-631468-g008.jpg

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