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抑制软腐病原菌RCE的群体感应机制,以调控其毒力因子和生物膜形成。

inhibits quorum-sensing mechanisms of soft rot pathogen RCE to regulate its virulence factors and biofilm formation.

作者信息

Kapadia Chintan, Kachhdia Rinkal, Singh Susheel, Gandhi Kelvin, Poczai Peter, Alfarraj Saleh, Ansari Mohammad Javed, Gafur Abdul, Sayyed R Z

机构信息

Department of Plant Molecular Biology and Biotechnology, ASPEE College of Horticulture and Forestry, Navsari Agricultural University, Navsari, India.

Food Quality Testing Laboratory, N. M. College of Agriculture, Navsari Agricultural University, Navsari, India.

出版信息

Front Microbiol. 2022 Aug 23;13:977669. doi: 10.3389/fmicb.2022.977669. eCollection 2022.

Abstract

The quorum-sensing (QS) cascade is responsible for the colonization and phenotypic behavior of the pathogenic organism and the regulation of diverse signal molecules. The disruption of the quorum-sensing system is an effective strategy to overcome the possibility of antibiotic resistance development in the pathogen. The quorum quenching does not kill the microbes. Instead, it hinders the expression of pathogenic traits. In the present experiment, RKC1 was used to extract the metabolites responsible for quorum-sensing inhibition in soft rot pathogen RCE. During the initial screening, RKC1 was found to be most promising and inhibits violacein of MTCC2656 pyocyanin, swarming-swimming motility of MTCC2297. The characterization of metabolites produced by the microbes which are responsible for quorum-sensing inhibition through GC-MS is very scarce in scientific literature. The ethyl acetate extract of RKC1 inhibits biofilm formation of RCE while inhibiting growth at higher concentrations. The GC-MS analysis suggested that Cyclic dipeptides (CDPs) such as Cyclo (L-prolyl-L-valine), Cyclo (Pro-Leu), and Cyclo(D-phenylalanyl-L-prolyl) were predominantly found in the ethyl acetate extract of the RKC1 (93.72%). This diketopiperazine (DKPs) exhibited quorum-sensing inhibition against the pathogen in liquid media during the active growth phase and regulated diverse metabolites of the pathogen. Moreover, the metabolites data from the clear zone around wells showed a higher concentration of DKSs (9.66%) compared to other metabolites. So far, very few reports indicate the role of DKPs or CDPs in inhibiting the quorum-sensing system in plant pathogenic bacteria. This is one such report that exploits metabolites of RKC1. The present investigation provided evidence to use quorum-sensing inhibitor metabolites, to suppress microbes' pathogenesis and thus develop an innovative strategy to overcome antibiotic resistance.

摘要

群体感应(QS)级联负责致病生物体的定殖和表型行为以及多种信号分子的调节。破坏群体感应系统是克服病原体产生抗生素耐药性可能性的有效策略。群体淬灭不会杀死微生物。相反,它会阻碍致病性状的表达。在本实验中,使用RKC1提取软腐病原菌RCE中负责群体感应抑制的代谢物。在初步筛选中,发现RKC1最具潜力,可抑制MTCC2656绿脓菌素的紫菌素、MTCC2297的群体游动运动。科学文献中关于通过气相色谱 - 质谱法表征负责群体感应抑制的微生物产生的代谢物的报道非常少。RKC1的乙酸乙酯提取物在抑制RCE生物膜形成的同时,在较高浓度下会抑制其生长。气相色谱 - 质谱分析表明,在RKC1的乙酸乙酯提取物中主要发现了环二肽(CDP),如环(L - 脯氨酰 - L - 缬氨酸)、环(脯氨酸 - 亮氨酸)和环(D - 苯丙氨酰 - L - 脯氨酰)(93.72%)。这种二酮哌嗪(DKP)在活跃生长阶段对液体培养基中的病原体表现出群体感应抑制作用,并调节病原体的多种代谢物。此外,来自孔周围透明区的代谢物数据显示,与其他代谢物相比,DKSs的浓度更高(9.66%)。到目前为止,很少有报告表明DKP或CDP在抑制植物病原细菌群体感应系统中的作用。这就是这样一份利用RKC1代谢物的报告。本研究为使用群体感应抑制剂代谢物来抑制微生物的致病性从而开发一种克服抗生素耐药性的创新策略提供了证据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1201/9450810/ac79c2ff3015/fmicb-13-977669-g0001.jpg

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