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Mechanisms of Antibiotic Resistance in Acinetobacter spp. — Genetics of Resistance
Published in E. Bergogne-Bénézin, M.L. Joly-Guillou, K.J. Towner, Acinetobacter, 2020
The fluorinated 4-quinolones must be regarded as one of the major contributions to the control of severe nosocomial infections caused by Gram-negative bacteria. As described in the previous chapter, the emergence of Acinetobacter spp. as important hospital pathogens has occurred at the same time as increased reliance on 4-quinolones for the treatment of serious infection. It is worth considering whether these two facts are coincidental, or whether the use of one leads to the other.
Antibiotics Commonly Used for Skin Infections
Published in Sarah H. Wakelin, Howard I. Maibach, Clive B. Archer, Handbook of Systemic Drug Treatment in Dermatology, 2015
Hui Min Liew, Victoria J. Hogarth, Roderick J. Hay
The fluoroquinolones or 4-quinolones are antibiotics whose principal use in dermatology is the treatment of Gram-negative infections. Their mode of action is by inhibition of DNA synthesis. Generally only one of these agents, ciprofloxacin, is used in dermatology. Other fluroquinolones include norfloxacin and ofloxacin.
Gut bacterial extracellular vesicles: important players in regulating intestinal microenvironment
Published in Gut Microbes, 2022
Xiao Liang, Nini Dai, Kangliang Sheng, Hengqian Lu, Jingmin Wang, Liping Chen, Yongzhong Wang
QS molecules are signaling substances used by bacteria to coordinate community behavior, such as regulating bacterial symbiosis and competition, influencing the secretion of bacterial metabolites and virulence factors, and regulating biofilm formation(Figure 2B).66 Currently, few studies have investigated the delivery of QS molecules by GBEVs. Of those studies, most have focused on the GBEVs secreted by the opportunistic pathogen Pseudomonas aeruginosa and the production of 2-heptyl-3-hydroxy-4-quinolone (Pseudomonas quinolone signal, PQS). These studies have suggested that the interaction between PQS and P. aeruginosa EVs can be considered “synergistic”. Cooke et al. found that most wild-type P. aeruginosa strains require induction by PQS to secrete GBEVs.67 Further, Bala et al. observed that GBEV production was significantly reduced in the pqs gene mutants of P. aeruginosa, and that exogenous supplementation with PQS induced a significant release of GBEVs by this strain again.54 The mechanism underlying PQS-containing GBEV (PQS-GBEV) production in P. aeruginosa broadly involves the insertion of PQS into the bacterial outer membrane, which leads to the expansion of the outer leaflet, resulting in the bending of the outer membrane and the eventual formation of PQS-GBEVs.68 Subsequently, PQS can enter other P. aeruginosa cells via GBEVs, thereby regulating the behavior of the P. aeruginosa population.
Subtle relationships between Pseudomonas aeruginosa and fungi in patients with cystic fibrosis
Published in Acta Clinica Belgica, 2022
Kaicheng Yan, Hong Yin, Jin Wang, Yun Cai
PA can produce more than 50 types of alkyl quinolones, and many of them have been proved to use 2-heptyl-3-hydroxy-4-quinolones [Pseudomonas quinolone signal (PQS)] and its direct precursor 2-heptyl-4-quinolones (HHQ) as signal molecules of intercellular communication [58]. Motility and biofilm formation in bacteria and fungi are repressed in the presence of HHQ. There is a significant reduction in the ability of CA to form biofilms in the presence of HHQ, revealing an interkingdom dimension to the HHQ function [59]. Similar effects on fungal morphology have been observed like other compounds that contain a 12-carbon backbone, and HHQ can inhibit the filamentation of yeast cells and cause filamentous cells to switch the growth as yeast cells [60]. Besides, the PQS system participates in the production of Rhls, eDNA, and biofilm formation [61].
Alternative approaches to treat bacterial infections: targeting quorum-sensing
Published in Expert Review of Anti-infective Therapy, 2020
Pipat Piewngam, Janice Chiou, Priyanka Chatterjee, Michael Otto
P. aeruginosa is a ubiquitous Gram-negative bacterium that naturally occurs in soil and water and an opportunistic pathogen that primarily infects immunocompromised individuals [85]. The LasI/R QS system, a homolog of the V. fischeri LuxI/R system is the first QS system of P. aeruginosa that has been described [4]. However, P. aeruginosa has later been found to express several other QS systems, including RhlI/R [86] and the PqsR-controlled quinolone system [87,88], which are arranged in a regulatory cascade with the LasI/R system on top. The lasI gene encodes the enzyme producing N-(3-oxo-dodecanoyl)-homoserine lactone (3-oxo-C12-HSL) [89], which binds and activates the cognate response regulator LasR [90,91], resulting in the regulation of target gene expression [91–93]. The LasR–AHL complex then stimulates expression of rhlR and rhlI [94,95], and the pqsR and pqsABCDE genes of the quinolone system [96]. RhlI synthesizes N-(butanoyl)-homoserine lactone (C4-HSL), which interacts with the cognate RhlR [97]. In addition, RhlR inhibits the expression of pqsR and pqsABCDE, and this loop is suggested to ensure the correct ratio of 3-oxo-C12-HSL to C4-HSL, which, in turn, dictates the activation of quinolone (2-heptyl-3-hydroxy-4-quinolone, known as PQS) [98].