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海洋细菌假交替单胞菌3J6对棕环病病原体塔氏弧菌的抗生物膜活性

Antibiofilm Activity of the Marine Bacterium Pseudoalteromonas sp. 3J6 Against Vibrio tapetis, the Causative Agent of Brown Ring Disease.

作者信息

Rodrigues Sophie, Paillard Christine, Dufour Alain, Bazire Alexis

机构信息

EA 3884, LBCM, IUEM, Univ. Bretagne-Sud, 56100, Lorient, France,

出版信息

Probiotics Antimicrob Proteins. 2015 Mar;7(1):45-51. doi: 10.1007/s12602-014-9173-3.

Abstract

Vibrio tapetis CECT4600 is a pathogenic Gram-negative bacterium causing the brown ring disease in the Manila clam Ruditapes philippinarum. This vibriosis is induced by bacterial attachment on the periostracal lamina, yielding a decalcification of the bivalve shell. As in many bacterial species, pathogenesis is likely related to biofilm formation. The proteinaceous exoproducts of the marine bacterium Pseudoalteromonas sp. 3J6 inhibit the formation of biofilm by most of the tested marine bacteria without affecting their planktonic growth. In the present work, we examined the sensitivity of V. tapetis to Pseudoalteromonas sp. 3J6 and its exoproducts. In V. tapetis CECT4600-GFP-Pseudoalteromonas sp. 3J6 co-cultures, the latter outcompeted V. tapetis whatever the growth mode (planktonic or biofilm), which could result from a slower growth of V. tapetis. Biofilms containing only V. tapetis were grown in vitro on a glass substratum under dynamic conditions. When the glass was coated with a culture supernatant of Pseudoalteromonas sp. 3J6 (SN(3J6)) prior to inoculating V. tapetis CECT4600-GFP, the bacterial attachment was about fivefold lower than in control experiment without SN3J6 and the biofilm formation was delayed by about 24 h: A full biofilm was obtained at 48 versus 24 h for the control. Moreover, a preformed V. tapetis biofilm (grown on SN(3J6)-free glass substratum) could be disrupted by incubating it with SN3J6. This data suggest that Pseudoalteromonas sp. 3J6 is a good candidate to set up an anti-V. tapetis strategy usable in aquaculture to grow V. tapetis-free Manila clam spats.

摘要

塔氏弧菌CECT4600是一种革兰氏阴性病原菌,可导致菲律宾蛤仔患褐环病。这种弧菌病是由细菌附着在贝壳外层薄片上引起的,会导致双壳贝类外壳脱钙。与许多细菌种类一样,发病机制可能与生物膜形成有关。海洋细菌假交替单胞菌属3J6的蛋白质外产物可抑制大多数受试海洋细菌生物膜的形成,而不影响其浮游生长。在本研究中,我们检测了塔氏弧菌对假交替单胞菌属3J6及其外产物的敏感性。在塔氏弧菌CECT4600-绿色荧光蛋白-假交替单胞菌属3J6共培养物中,无论生长模式(浮游或生物膜)如何,后者都比塔氏弧菌更具竞争力,这可能是由于塔氏弧菌生长较慢所致。仅含塔氏弧菌的生物膜在动态条件下于玻璃基质上进行体外培养。在接种塔氏弧菌CECT4600-绿色荧光蛋白之前,用假交替单胞菌属3J6的培养上清液(SN(3J6))包被玻璃,细菌附着量比无SN3J6的对照实验低约五倍,生物膜形成延迟约24小时:对照在24小时形成完整生物膜,而此时处理组在48小时才形成。此外,预先形成的塔氏弧菌生物膜(在无SN(3J6)的玻璃基质上生长)与SN3J6一起孵育时会被破坏。这些数据表明,假交替单胞菌属3J6是制定一种可用于水产养殖的抗塔氏弧菌策略的良好候选菌株,以培育无塔氏弧菌的菲律宾蛤仔幼贝。

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