Abstract :
As widely distributed Gram-negative bacilli, Serratia marcescens is in soil, vegetation, food and aquatic environments as well as human tissues. S. marcescens is well known for its opportunistic pathogenicity, regularly influencing immunocompromised individuals. This pathogen employs cell to cell communication system known as quorum sensing (QS) to coordinate multiple physiological and virulence activities via controlling the gene expression of involved determinants through three major systems referred to as SwrIR, SmaIR, and SpnIR.
In S. marcescens the core autoinducers comprise N-acyl-homoserine lactones (AHLs), with N-butanoyl-L-homoserine lactone (BHL) being the main one. These autoinducers combine with LuxR-analogue receptors (e.g. SmaR) that lead to initiate the gene expression modifications; thereby starting various coordinated behaviours.
Thorough awareness of QS strategies is considered imperative for developing techniques to alleviate the pathogenicity of S. marcescens, principally in clinical facilities in which it exerts considerable challenges owing to its multidrug resistance as well as its capacity to establish recalcitrant biofilms. Upon that, the current review explores the QS mechanisms of S. marcescens, aiming to uncover novel methods to alleviate its harmful consequences.
Keywords :
AHL, quorum sensing, Serratia marcescens, SmaI/SmaR, SpnI/SpnR, SwrI/SwrRReferences :
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