Mechanisms and Targeted Therapies forPseudomonas aeruginosaLung Infection
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Abstract:
Pseudomonas aeruginosa is a complex gram-negative facultative anaerobe replete with a variety of arsenals to activate, modify, and destroy host defense mechanisms. The microbe is a common cause of nosocomial infections and an antibiotic-resistant priority pathogen. In the lung, P. aeruginosa disrupts upper and lower airway homeostasis by damaging the epithelium and evading innate and adaptive immune responses. The biology of these interactions is essential to understand P. aeruginosa pathogenesis. P. aeruginosa interacts directly with host cells via flagella, pili, lipoproteins, lipopolysaccharides, and the type III secretion system localized in the outer membrane. P. aeruginosa quorum-sensing molecules regulate the release of soluble factors that enhance the spread of infection. These characteristics of P. aeruginosa differentially affect lung epithelial, innate, and adaptive immune cells involved in the production of mediators and the recruitment of additional immune cell subsets. Pathogen interactions with individual host cells and in the context of host acute lung infection are discussed to reveal pathways that may be targeted therapeutically.Cite
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Pseudomonas aeruginosa is an opportunistic pathogen with severe antibiotic resistance problems, challenging the use of traditional antibiotics. Quorum sensing is a phenomenon of cell density dependent control of gene expression which controls the expression of virulence factors and biofilm formation in pseudomonas aeruginosa. Inhibition of quorum sensing can reduce the virulence of pseudomonas aeruginosa but shows no selection pressure thus making it a potential anti-infection strategy which is less likely to cause resistance. This review presents the research progress of pseudomonas aeruginosa quorum sensing inhibitors in recent years.
Key words:
Pseudomonas aeruginosa; Quorum sensing; Inhibitor
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Diastereomeric 2-methoxycyclopentyl analogues of a natural quorum sensing signaling molecule from Pseudomonas aeruginosa were synthesized and screened in pigment production assays with P. aeruginosa and Serratia strain ATCC39006.
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Pseudomonas aeruginosa has two complete quorum-sensing systems. Both of these systems have been shown to be important for Pseudomonas virulence in multiple models of infection. Thus, these systems provide unique targets for novel antimicrobial drugs.
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P SEUDOMONAS aeruginosa is an important opportunistic human pathogen that causes serious infection diseases.The quorum sensing (QS) system is a cell to cell signaling mechanism that it has important role in the regulating of bacterial genes.Pseudomonas aeruginosa has two important QS systems including lasIR and rhlIR.Therefore, our aim was introduced these systems in the topic bacteria P. aeruginosa.
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Antagonism of quorum sensing represents a promising new antivirulence approach for the treatment of bacterial infection. The development of a novel series of non-natural irreversible antagonists of P. aeruginosa LasR is described. The lead compounds identified (25 and 28) display potent LasR antagonist activity and inhibit expression of the P. aeruginosa virulence factors pyocyanin and biofilm formation in PAO1 and PA14.
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