About this Research Topic
We welcome you to submit your manuscripts on quorum networks (sensing/quenching) and their relationship with drug resistance in pathogens. Since studies about these mechanisms in multidrug-resistant pathogens are scarce, it is necessary to increase our understanding in this field.
Quorum sensing (QS) is a general mechanism used by Gram-negative and Gram-positive bacteria to regulate many biological processes, including virulence, competence, conjugation, resistance, motility and biofilm formation. Several important bacterial pathogens, like Pseudomonas aeruginosa, Staphylococcus aureus, and Vibrio cholerae, utilize QS cell communication to coordinate the expression of multiple virulence factors and associated behaviors such as swarming and biofilm formation, once a population size threshold is reached. QS systems consist of an enzyme that catalyzes the synthesis of a signal (such as acyl-homoserine lactones or cyclic peptides) and a receptor that binds the signal and reprograms the expression of several genes, including those encoding the enzyme that produces the signal, creating a positive feedback loop. In bacterial pathogens, most of the QS-controlled genes codify several different virulence factors, such as proteases, toxins, and adhesin. The expression of QS-controlled phenotypes is energetically costly to bacteria and only provides an advantage if it is expressed when cells reach high densities.
Quorum quenching (QQ) can effectively interfere with any one of the key processes in QS, and this could potentially be exploited to treat and prevent microbial infections (e.g. inhibition of motility, toxin production, and biofilm formation). Naturally-occurring QQ mechanisms act by blocking the key steps of QS, such as signal generation, signal accumulation and signal reception. Microorganisms exist in a multi-species, competitive environment and have developed many survival strategies, including QQ, to gain benefits and compete for space, nutrition and ecological niches.
Therefore, the findings of the contributed studies must reflect some aspect of (QS/QQ) in multidrug-resistant pathogens, including, but not restricted to, those that describe (i) novel mechanisms of QS, (ii) QS/QQ in clinical multidrug resistant strains, (iii) the relationship between QS/QQ and multidrug resistance, and (iv) the application of new QQ therapies.
Quorum sensing (QS) is a general mechanism used by Gram-negative and Gram-positive bacteria to regulate many biological processes, including virulence, competence, conjugation, resistance, motility and biofilm formation. Several important bacterial pathogens, like Pseudomonas aeruginosa, Staphylococcus aureus, and Vibrio cholerae, utilize QS cell communication to coordinate the expression of multiple virulence factors and associated behaviors such as swarming and biofilm formation, once a population size threshold is reached. QS systems consist of an enzyme that catalyzes the synthesis of a signal (such as acyl-homoserine lactones or cyclic peptides) and a receptor that binds the signal and reprograms the expression of several genes, including those encoding the enzyme that produces the signal, creating a positive feedback loop. In bacterial pathogens, most of the QS-controlled genes codify several different virulence factors, such as proteases, toxins, and adhesin. The expression of QS-controlled phenotypes is energetically costly to bacteria and only provides an advantage if it is expressed when cells reach high densities.
Quorum quenching (QQ) can effectively interfere with any one of the key processes in QS, and this could potentially be exploited to treat and prevent microbial infections (e.g. inhibition of motility, toxin production, and biofilm formation). Naturally-occurring QQ mechanisms act by blocking the key steps of QS, such as signal generation, signal accumulation and signal reception. Microorganisms exist in a multi-species, competitive environment and have developed many survival strategies, including QQ, to gain benefits and compete for space, nutrition and ecological niches.
Therefore, the findings of the contributed studies must reflect some aspect of (QS/QQ) in multidrug-resistant pathogens, including, but not restricted to, those that describe (i) novel mechanisms of QS, (ii) QS/QQ in clinical multidrug resistant strains, (iii) the relationship between QS/QQ and multidrug resistance, and (iv) the application of new QQ therapies.
Keywords: Quorum Sensing, Quorum Quenching, Multidrug-resistant, Pathogens
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