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有机酸可减轻无乳链球菌在罗非鱼肠道原代细胞和肠道感染模型中的毒力。

Organic acids mitigate Streptococcus agalactiae virulence in Tilapia fish gut primary cells and in a gut infection model.

作者信息

Liliana Petculescu Ciochina, Dumitrescu Gabi, McCleery David, Pet Ioan, Iancu Tiberiu, Stef Lavinia, Corcionivoschi Nicolae, Balta Igori

机构信息

Faculty of Bioengineering of Animal Resources, University of Life Sciences King Mihai I from Timisoara, Timisoara, 300645, Romania.

Bacteriology Branch, Veterinary Sciences Division, Agri-Food and Biosciences Institute, Northern Ireland, Belfast, BT4 3SD, UK.

出版信息

Ir Vet J. 2024 May 27;77(1):10. doi: 10.1186/s13620-024-00272-1.

DOI:10.1186/s13620-024-00272-1
PMID:38797844
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11129440/
Abstract

BACKGROUND

Streptococcus agalactiae, a Gram-positive bacterium, has emerged as an important pathogen for the aquaculture industry worldwide, due to its increased induced mortality rates in cultured fish. Developing interventions to cure or prevent infections based on natural alternatives to antibiotics has become a priority, however, given the absence of scientific evidence regarding their mode of action progress has been slow.

METHODS

In this study we aimed to investigate the effect of a mixture of organic acids (natural antimicrobials), AuraAqua (Aq), on the virulence of S. agalactiae using Tilapia gut primary epithelial cells and an in vitro Tilapia gut culture model. Our results show that Aq was able to reduce significantly, in vitro, the S. agalactiae levels of infection in Tilapia gut primary epithelial cells (TGP) when the MIC concentration of 0.125% was tested.

RESULTS AND DISCUSSION

At bacterial level, Aq was able to downregulate bacterial capsule polysaccharide (CPS) gene expression, capC, resulting in a significant decrease in bacterial surface capsule production. The decrease in CPS production was also associated with a reduction in the pro-inflammatory IFNγ, IL1β, TNFα, SOD and CAT gene expression and HO production in the presence of 0.125% Aq (P < 0.0001). The antimicrobial mixture also reduced the levels of S. agalactiae infection in an in vitro gut culture model and significantly reduced the IFNγ, IL1β, TNFα, SOD, CAT gene expression and HO production in infected tissue. Moreover, genes involved in Tilapia resistance to S. agalactiae induced disease, MCP-8 and Duo-1, were also downregulated by Aq, as a consequence of reduced bacterial levels of infection.

CONCLUSION

Conclusively, our study shows that mixtures of organic acids can be considered as potential alternative treatments to antibiotics and prevent S. agalactiae infection and inflammation in the Tilapia fish digestive tract.

摘要

背景

无乳链球菌是一种革兰氏阳性菌,由于其在养殖鱼类中导致的死亡率上升,已成为全球水产养殖业的一种重要病原体。鉴于缺乏关于其作用方式的科学证据,开发基于抗生素天然替代品的治疗或预防感染的干预措施已成为当务之急,但进展缓慢。

方法

在本研究中,我们旨在使用罗非鱼肠道原代上皮细胞和体外罗非鱼肠道培养模型,研究有机酸混合物(天然抗菌剂)AuraAqua(Aq)对无乳链球菌毒力的影响。我们的结果表明,当测试0.125%的最低抑菌浓度(MIC)时,Aq能够在体外显著降低罗非鱼肠道原代上皮细胞(TGP)中无乳链球菌的感染水平。

结果与讨论

在细菌水平上,Aq能够下调细菌荚膜多糖(CPS)基因capC的表达,导致细菌表面荚膜产量显著降低。在存在0.125% Aq的情况下,CPS产量的降低还与促炎细胞因子IFNγ、IL1β、TNFα、超氧化物歧化酶(SOD)和过氧化氢酶(CAT)基因表达以及过氧化氢(HO)产生的减少有关(P < 0.0001)。抗菌混合物在体外肠道培养模型中也降低了无乳链球菌的感染水平,并显著降低了感染组织中IFNγ、IL1β、TNFα、SOD、CAT基因表达和HO产生。此外,由于细菌感染水平降低,参与罗非鱼抵抗无乳链球菌诱导疾病的基因MCP - 8和Duo - 1也被Aq下调。

结论

总之,我们的研究表明,有机酸混合物可被视为抗生素的潜在替代治疗方法,并可预防罗非鱼消化道中的无乳链球菌感染和炎症。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9309/11129440/ea817891546d/13620_2024_272_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9309/11129440/22f7ccfd6456/13620_2024_272_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9309/11129440/d9a1b44ca82a/13620_2024_272_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9309/11129440/7e6821b83e16/13620_2024_272_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9309/11129440/5d0eb6e3ff2e/13620_2024_272_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9309/11129440/5069eb506403/13620_2024_272_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9309/11129440/ea817891546d/13620_2024_272_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9309/11129440/22f7ccfd6456/13620_2024_272_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9309/11129440/d9a1b44ca82a/13620_2024_272_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9309/11129440/7e6821b83e16/13620_2024_272_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9309/11129440/5d0eb6e3ff2e/13620_2024_272_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9309/11129440/5069eb506403/13620_2024_272_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9309/11129440/ea817891546d/13620_2024_272_Fig6_HTML.jpg

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