article · Microorganisms
Serratia marcescens is a hospital-acquired bacterial pathogen that causes severe wound and burn infections and displays high antibiotic resistance. Targeting quorum sensing offers an alternative therapy by reducing bacterial virulence without exerting selective survival pressure. Testing shows that the sugar alcohol xylitol inhibits the growth of S. marcescens and, at sub-inhibitory levels, curbs its ability to form protective biofilms, move via swimming or swarming, and produce prodigiosin and proteases. Xylitol also increases the pathogen's vulnerability to hydrogen peroxide and downregulates several critical genes governing virulence. Computational analysis indicates that xylitol binds to the SmaR receptor, disrupting natural quorum-sensing signals. Furthermore, an in vivo survival assay in mice demonstrated that xylitol protects against bacterial virulence, showing its potential as an agent to treat S. marcescens wound and burn infections.
Serratia marcescens causes hospital-acquired wound and burn infections that are increasingly hard to treat with conventional antibiotics. By interfering with quorum-sensing communication rather than simply killing bacteria, antivirulence agents like xylitol can disarm pathogens and make them vulnerable to the host immune system. This strategy provides a promising alternative approach to managing drug-resistant bacterial infections in clinical care settings.
The findings point to the potential development of xylitol-based topical formulations or therapeutics to manage Serratia marcescens infections in wounds and burns. Such treatments would be of interest to wound care specialists, hospitals, and pharmaceutical companies developing antivirulence therapies. Given that testing remains at the laboratory stage using computational models and early in vivo mouse survival assays, the research is early-stage and requires further preclinical evaluation before clinical translation.
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<i>Serratia marcescens</i> is an opportunistic nosocomial pathogen and causes wound and burn infections. It shows high resistance to antibiotics and its pathogenicity is mediated by an arsenal of virulence factors. Another therapeutic option to such infections is targeting quorum sensing (QS), which controls the expression of different <i>S. marcescens</i> virulence factors. Prevention of QS can deprive <i>S. marcescens</i> from its bacterial virulence without applying stress on the bacterial growth and facilitates the eradication of the bacteria by immunity. The objective of the current study is to explore the antimicrobial and antivirulence activities of xylitol against <i>S. marcescens</i>. Xylitol could inhibit the growth of <i>S. marcescens</i>. Sub-inhibitory concentrations of xylitol could inhibit biofilm formation, reduce prodigiosin production, and completely block protease activity. Moreover, xylitol decreased swimming motility, swarming motility and increased the sensitivity to hydrogen peroxide. The expression of <i>rsmA</i>, <i>pigP</i>, <i>flhC</i>, <i>flhD fimA</i>, fimC, <i>shlA bsmB</i>, and <i>rssB</i> genes that regulate virulence factor production was significantly downregulated by xylitol. In silico study showed that xylitol could bind with the SmaR receptor by hydrophobic interaction and hydrogen bonding, and interfere with the binding of the natural ligand with SmaR receptor. An in vivo mice survival test confirmed the ability of xylitol to protect mice against the virulence of <i>S. marcescens</i>. In conclusion, xylitol is a growth and virulence inhibitor in <i>S. marcescens</i> and can be employed for the treatment of <i>S. marcescens</i> wound and burn infections.
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DOI: 10.3390/microorganisms9051083
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