Articles

The Role of Potassium Silicate in Quorum Quenching Against the Virulence of Ralstonia solanacearum, the Causal Agent of Bacterial Wilt in Tomato

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Bacterial wilt caused by Ralstonia solanacearum remains one of the most destructive constraints in tomato production worldwide. The pathogen’s virulence is tightly regulated by quorum sensing (QS), which controls exopolysaccharide (EPS) biosynthesis, extracellular enzyme secretion, and biofilm formation. Targeting QS through quorum quenching (QQ) represents a promising anti-virulence strategy without imposing the selective pressure associated with conventional bactericides. This study investigated the dual role of potassium silicate as (i) a QS-interfering agent that modulates bacterial virulence traits and (ii) an inducer of host systemic resistance. Potassium silicate at 1 mM significantly reduced EPS production and biofilm formation, whereas 2 mM enhanced peroxidase activity in tomato plants. Disease severity was reduced during the early stages of infection in silica-treated plants. These findings indicate that potassium silicate attenuates bacterial wilt development through the integrated modulation of pathogen virulence and host defense responses. This study provides mechanistic insight into silicon-mediated plant protection and highlights potassium silicate as a sustainable strategy for bacterial wilt management.

Serratia marcescens whispering world: Mechanisms and Implications

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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.