Resistance Is Not Futile: The Role of Quorum Sensing Plasticity in Pseudomonas aeruginosa Infections and Its Link to Intrinsic Mechanisms of Antibiotic Resistance.
Resistance Is Not Futile: The Role of Quorum Sensing Plasticity in Pseudomonas aeruginosa Infections and Its Link to Intrinsic Mechanisms of Antibiotic Resistance.
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抗性并非徒劳：群体感应可塑性在铜绿假单胞菌感染中的作用及其与抗生素耐药性内在机制的联系。
DOI：
10.3390/microorganisms10061247
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发表时间：
2022-06-18
期刊：
影响因子：
4.5
通讯作者：
中科院分区：
文献类型：
--
作者：
细菌使用称为群体感应（QS）的细胞间通信过程来协调集体行为。QS依赖于对称为自诱导物（AI）的细胞外信号分子的全组检测。群体感应是人类病原体铜绿假单胞菌毒力和生物膜形成所必需的。在铜绿假单胞菌中，LasR和RhIR是同源LuxR型可溶性转录因子受体，其结合其同源AI并激活编码毒力和生物膜形成所需功能的基因的表达。虽然一些细菌信号转导途径遵循线性回路，因为磷酰基基团从一种载体蛋白传递到另一种载体蛋白，最终导致靶基因的上调或下调，但铜绿假单胞菌中的QS系统是具有相互连接的调节系统和输出的受体和调节剂的密集网络。一旦被激活，不清楚LasR和RhlR如何建立它们的信号传导层级，也不清楚这些通路连接如何被调节，从而导致慢性感染。在这里，我们综述了QS进展的机制，因为它涉及到细菌的发病机制和抗生素耐药性和耐受性。
Bacteria use a cell-cell communication process called quorum sensing (QS) to orchestrate collective behaviors. QS relies on the group-wide detection of extracellular signal molecules called autoinducers (AI). Quorum sensing is required for virulence and biofilm formation in the human pathogen Pseudomonas aeruginosa. In P. aeruginosa, LasR and RhlR are homologous LuxR-type soluble transcription factor receptors that bind their cognate AIs and activate the expression of genes encoding functions required for virulence and biofilm formation. While some bacterial signal transduction pathways follow a linear circuit, as phosphoryl groups are passed from one carrier protein to another ultimately resulting in up- or down-regulation of target genes, the QS system in P. aeruginosa is a dense network of receptors and regulators with interconnecting regulatory systems and outputs. Once activated, it is not understood how LasR and RhlR establish their signaling hierarchy, nor is it clear how these pathway connections are regulated, resulting in chronic infection. Here, we reviewed the mechanisms of QS progression as it relates to bacterial pathogenesis and antimicrobial resistance and tolerance.
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