Abstract

Rapid emergence of antimicrobial resistance (AMR) has become a critical challenge worldwide. It is of great importance to understand how AMR is modulated genetically in order to explore new antimicrobial strategies. Recent studies have unveiled that microbial communication systems, which are known to play key roles in regulation of bacterial virulence, are also associated with the formation and regulation of AMR. These microbial cell-to-cell chemical communication systems, including quorum sensing (QS) and pathogen–host communication mechanisms, rely on detection and response of various chemical signal molecules, which are generated either by the microbe itself or host cells, to activate the expression of virulence and AMR genes. This article summarizes the generic signaling mechanisms of representative QS and pathogen–host communications systems, reviews the current knowledge regarding the roles of these chemical communication systems in regulation of AMR, and describes the strategies developed over the years for blocking bacterial chemical communication systems in disease control. The research progress in this field suggests that the bacterial cell-cell communication systems are a promising target not only for disease control but also for curbing the problem of microbial drug resistance.

Highlights

  • Pathogenic microorganisms are one of the major threats to the life quality of living organisms, including humans, animals and plants

  • Different bacterial species produce similar AHL signaling molecules with a conserved N-acyl homoserine lactone, but the fatty acid side chain lengths and substituents are in general variable, which may account for their signaling specificity in different microorganisms [66]

  • A wide range of microbial biological functions are known to be regulated by the AHL quorum sensing (QS) system, including bioluminescence, plasmid DNA transfer, production of pathogenic factors, biofilm formation, and antibiotic production [23]

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Summary

Introduction

Pathogenic microorganisms are one of the major threats to the life quality of living organisms, including humans, animals and plants. Rapid increase in AMR problems highlights the need of searching for new strategies or alternative approaches to prevent formation and spreading AMR, or sensitize pathogenic microorganisms to conventional antibiotics. In this regard, understanding the potential molecular mechanisms associated with modulation of AMR may hold the key to unlock the AMR problem. Since 1990s, it has become known that numerous microbial activities, including plasmid conjugal transfer, virulence factor production, biofilm formation, and expression of efflux pumps, are regulated by microbial cell-cell communication mechanisms, including QS and pathogen–host chemical signaling systems [24,25,26,27]. Evidence is emerging that blocking these microbial cell-cell communication systems could provide effective control against microbial infections, highlighting a promising potential to curb the emerging AMR problems

Overview of Antimicrobial and AMR Mechanisms
Fundamentals of Microbial Chemical Communication Systems
AHL-Type QS System
DSF-Type QS System
Polyamine-Mediated Host–Pathogen Communication Systems
The Role of the AHL QS System in Modulation of Antibiotic Resistance
The Role of DSF QS System in Modulation of Antibiotic Resistance
The of Polyamine the Polyamine
Strategies for Blocking Microbial Chemical Communication Systems
Findings
Conclusions and Future Prospective
Full Text
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