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副溶血性弧菌外膜孔蛋白Vpa0810调节其生物膜形成,并在其应激耐受性中发挥重要作用。

Vibrio parahaemolyticus outer membrane porin Vpa0810 regulates its biofilm formation and plays a vital role in its stresses tolerance.

作者信息

Sun Yu, Chu Min, Zhuhuang Chenzhi, Wang Yan, Mo Qiufen, Ni Qinxue, Zhang Youzuo, Yang Menghua, Xu Guangzhi

机构信息

College of Food and Health, Zhejiang A & F University, Zhejiang, Hangzhou 311300, China.

College of Food and Health, Zhejiang A & F University, Zhejiang, Hangzhou 311300, China.

出版信息

Int J Food Microbiol. 2025 Nov 2;442:111390. doi: 10.1016/j.ijfoodmicro.2025.111390. Epub 2025 Aug 14.

Abstract

Vibrio parahaemolyticus (V. parahaemolyticus), a Gram-negative halophilic bacterium, is a leading seafood-borne pathogen that can cause acute gastroenteritis. Outer membrane (OM) porins are involved in exporting extracellular polymeric substances, which is essential for biofilm formation. However, the contribution of porins to the biofilm formation of V. parahaemolyticus is still obscure. We recently found that a mutation in the DHH/DHHA1 family gene vp2835 enhances biofilm formation in V. parahaemolyticus but inhibits its motility. Here, we identified an OM porin gene, vpa0810, from Δvp2835 strain. The deletion of vpa0810 in the wild type strain resulted in the inhibition of both swarming and swimming motility, while reverted the motility defect of Δvp2835. The Δvpa0810 decreased its biofilm formation capability in both the wild type and the Δvp2835 strain. Additionally, the surface hydrophobicity, auto-aggregation, OM permeability, and exopolysaccharides (EPS) content were decreased in the Δvpa0810 strain. Interestingly, qRT-PCR results demonstrated that the genes involved in EPS synthesis (cpsA, scvE, and cpsF) and the porin gene ompW were significantly up-regulated in the Δvpa0810 strain, but down-regulated in the Δvp2835-Δvpa0810 double mutant. Furthermore, the deletion of vpa0810 compromised its ability to form biofilm on silicon wafers, glass, stainless-steel plates, as well as on shrimp and crab surfaces. The vpa0810 deletion mutation also reduced its stress tolerance to bile salt, low pH, low temperature, and the antibiotics colistin. In summary, our data suggest that Vpa0810 may regulate biofilm formation through EPS biosynthesis and exportation, which might provide a new target for developing control strategies against V. parahaemolyticus.

摘要

副溶血性弧菌是一种革兰氏阴性嗜盐菌,是导致急性肠胃炎的主要食源性病原体。外膜孔蛋白参与细胞外聚合物的输出,这对生物膜形成至关重要。然而,孔蛋白对副溶血性弧菌生物膜形成的作用仍不清楚。我们最近发现,DHH/DHHA1家族基因vp2835中的一个突变增强了副溶血性弧菌的生物膜形成,但抑制了其运动性。在此,我们从Δvp2835菌株中鉴定出一个外膜孔蛋白基因vpa0810。野生型菌株中vpa0810的缺失导致群游和游动运动性均受到抑制,同时恢复了Δvp2835的运动缺陷。Δvpa0810降低了野生型和Δvp2835菌株的生物膜形成能力。此外,Δvpa0810菌株的表面疏水性、自聚集性、外膜通透性和胞外多糖(EPS)含量均降低。有趣的是,qRT-PCR结果表明,参与EPS合成的基因(cpsA、scvE和cpsF)和孔蛋白基因ompW在Δvpa0810菌株中显著上调,但在Δvp2835-Δvpa0810双突变体中下调。此外,vpa0810的缺失损害了其在硅片、玻璃、不锈钢板以及虾和蟹表面形成生物膜的能力。vpa0810缺失突变还降低了其对胆盐、低pH、低温和抗生素黏菌素的应激耐受性。总之,我们的数据表明,Vpa0810可能通过EPS生物合成和输出调节生物膜形成,这可能为开发针对副溶血性弧菌的控制策略提供新靶点。

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