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首页> 外文期刊>Microbial Pathogenesis >pH-dependent inhibition of AHL-mediated quorum sensing by cell-free supernatant of lactic acid bacteria in Pseudomonas aeruginosa PAO1
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pH-dependent inhibition of AHL-mediated quorum sensing by cell-free supernatant of lactic acid bacteria in Pseudomonas aeruginosa PAO1

机译:PSSudomonas铜绿假单胞菌PAO1中乳酸菌无细胞上清液抑制AHL介导的仲裁感测

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摘要

Antibiotic mediated therapies target the growth-related processes of the pathogen hence imparting a strong selection pressure on the pathogen to develop antibiotic resistance. Recently anti-virulence strategies have gained lots of attention amongst the scientific community, wherein instead of inhibiting the normal growth of pathogens, it interferes with the regulation of virulence factors of the pathogens and impede their pathogenesis. In Pseudomonas aeruginosa, the virulence mechanism accountable for various types of infections in humans depends on N-acyl homoserine lactone (AHL) mediated quorum sensing. So quenching of these molecules, pose as a promising tool against P. aeruginosa pathogenesis. Lactic acid bacteria cell-free supernatant (acidic and neutralized) were evaluated in quorum quenching of P. aeruginosa PAO1 (MTCC 3541) after their initial screening for anti-biofilm potential against this pathogen.Though the reduction in biofilm formation with acidic and neutralized supernatants of lactic acid bacteria revealed strain specific response but acidic fractions showed much stronger (P <= 0.05) inhibition of biofilm irrespective of the type of challenge given to P. aeruginosa with lactic acid bacteria. The acidic fraction of supernatants (L. lactis, L. rhamnosus and L. fermentum) not only showed a significant reduction (P <= 0.05) in auto-inducer AHL levels but also diminished elastase activity which was among important virulence characters directly controlled by the quorum sensing signaling. Moreover, significant decrease (P <= 0.05) in mRNA expression of last and rhil in presence of acidic fractions of lactic acid bacterial supernatants further confirmed the quorum quenching process in P. aeruginosa.
机译:抗生素介导的疗法靶向病原体的生长相关过程,因此赋予病原体的强烈选择压力以产生抗生素抗性。最近,抗毒力策略在科学界中获得了很多注意力,而是抑制病原体的正常生长,它干扰了病原体的毒力因子并妨碍了其发病机制。在假单胞菌铜绿假单胞菌中,对人类各种类型感染负责的毒力机制取决于N-酰基均静脉内酯(AHL)介导的仲裁感测。因此,使这些分子淬火,作为对P.铜绿假单胞菌发病机制的有前途的工具。在对该病原体的抗生物膜潜力的初始筛选后,评估乳酸菌细胞上清液(酸性和中和)在P.铜绿假单胞菌PaO1(MTCC 3541)的Quorum猝灭中。虽然用酸性和中和上清液的生物膜形成还原乳酸菌显示出菌株的响应,但酸性级分表现出更强的(P <= 0.05)生物膜的抑制,而不论与乳酸菌P.铜绿假单胞菌给出的攻击类型。上清液(L.乳酸,L. rhamnosus和L.Fermentum)的酸性级分不仅显示自动诱导剂AHL水平的显着减少(P <= 0.05),而且还减少了直接控制的重要毒力字符中的弹性蛋白酶活性减少法定传感信令。此外,在乳酸菌上清液的酸性级分的存在下,在乳酸细菌上清液存在下的mRNA表达中显着降低(P <= 0.05)进一步证实了P.铜绿假单胞菌的法定猝灭方法。

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