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Inhibition of biofilm formation and quorum sensing mediated virulence in Pseudomonas aeruginosa by marine sponge symbiont Brevibacterium casei strain Alu 1
Microbial Pathogenesis ( IF 3.3 ) Pub Date : 2020-12-24 , DOI: 10.1016/j.micpath.2020.104693
Nagasundaram Rashiya 1 , Nagarajan Padmini 1 , Antony Alex Kennedy Ajilda 1 , Pandiyan Prabakaran 2 , Ravindran Durgadevi 3 , Arumugam Veera Ravi 3 , Sougata Ghosh 4 , Natesan Sivakumar 5 , Gopal Selvakumar 1
Affiliation  

The alternative antimicrobial strategies that mitigate the threat of antibiotic resistance is the quorum-sensing inhibition (QSI) mechanism, which targets autoinducer dependent virulence gene expression in bacterial pathogens. N-acyl homoserine lactone (AHL) acts as a key regulator in the production of virulence factors and biofilm formation in Pseudomonas aeruginosa PAO1 and violacein pigment production in Chromobacterium violaceum ATCC 12472. In the present study, the marine sponge Haliclona fibulata symbiont Brevibacterium casei strain Alu 1 showed potential QSI activity in a concentration-dependent manner (0.5–2% v/v) against the N-acyl homoserine lactone (AHL)-mediated violacein production in C. violaceum (75–95%), and biofilm formation (53–96%), protease (27–82%), pyocyanin (82–95%) and pyoverdin (29–38%) productions in P. aeruginosa. Further, the microscopic analyses validated the antibiofilm activity of the cell-free culture supernatant (CFCS) of B. casei against P. aeruginosa. Subsequently, the biofilm and pyoverdin inhibitory efficacy of the ethyl acetate extract of B. casei CFCS was assessed against P. aeruginosa. Further, the gas chromatography–mass spectrometry (GC-MS) analysis revealed the presence of variety of components in which diethyl phthalate was found to be a major active component. This phthalate ester, known as diethyl ester of phthalic acid, could act as a potential therapeutic agent for preventing bacterial biofilm and virulence associated infectious diseases.



中文翻译:

海洋海绵共生干酪短杆菌菌株Alu 1对铜绿假单胞菌的生物膜形成和群体感应介导的毒力的抑制

减轻抗生素耐药性威胁的替代抗菌策略是群体感应抑制(QSI)机制,该机制的目标是细菌病原体中自诱导物依赖性毒力基因的表达。N-酰基高丝氨酸内酯(AHL)在铜绿假单胞菌PAO1中毒力因子的产生和生物膜形成以及紫罗兰色杆菌ATCC 12472中的紫胶素色素生产中起关键调节剂的作用在本研究中,海洋海绵腓肠杆菌共生干酪短杆菌菌株Alu 1对N-酰基高丝氨酸内酯(AHL)介导的紫胶素生产产生了浓度依赖性(0.5-2%v / v)的潜在QSI活性。C.堇色(75-95%),并且生物膜形成(53-96%),蛋白酶(27-82%),绿脓素(82-95%)和pyoverdin(29-38%)中制作的铜绿假单胞菌。此外,显微分析证实了干酪乳杆菌的无细胞培养上清液(CFCS)对铜绿假单胞菌的抗生物膜活性。随后,评估了干酪乳杆菌CFCS乙酸乙酯提取物对铜绿假单胞菌的生物膜和pyoverdin抑制作用。此外,气相色谱-质谱(GC-MS)分析表明存在多种成分,其中邻苯二甲酸二乙酯是主要的活性成分。这种邻苯二甲酸酯,被称为邻苯二甲酸二乙酯,可以作为预防细菌生物膜和毒力相关的传染病的潜在治疗剂。

更新日期:2021-01-03
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