TL;DR
Findings suggest that Withaferin A and Obacunone could serve as promising therapeutic agents against H. pylori infections by disrupting quorum sensing and biofilm formation, thus addressing the challenge of antibiotic resistance in this pathogen.
Recent structural and mechanistic insights into LuxR-type receptor function are summarized, including interactions with small molecules, protein partners, and DNA, including interactions with small molecules, protein partners, and DNA.
The Quorum Sensing (QS) system plays a central role in regulating several processes that influence bacterial physiology, communication, and pathogenesis. It governs the production of virulence factors, facilitates biofilm formation, and contributes to the development of antibiotic resistance, all of which are critical to bacterial survival and pathogenicity. QS enables both intraspecies and inter-species bacterial communication, operating through distinct pathways in Gram-positive and Gram-negative bacteria. This review provides a comprehensive overview of the major families of quorum-sensing proteins involved in the working of the signalling molecules. It examines the structural features, functional roles, and mechanisms of action of these proteins, highlighting their significance in bacterial behaviour. Furthermore, the study explores the potential of plant-derived secondary metabolites as natural inhibitors targeting QS systems to disrupt bacterial pathogenicity. Finally, it discusses the implications of exploiting these inhibitors as promising strategies to address the growing challenge of antibiotic resistance in bacterial infections.
This review highlights recent advances in the development of sulfonyl- and sulfinyl-containing organosulfur compounds as modulators of QS and biofilm formation in clinically relevant Gram-negative pathogens.
Summary Quorum sensing enables bacteria to coordinate collective behaviors crucial for survival and infection. Here, we show that Salmonella Typhimurium employs LuxS/autoinducer-2 (AI-2) signaling to regulate multiple stages of pathogenesis. AI-2 functions as a chemoattractant and modulates the expression of chemotaxis and motility-associated genes, promoting flagellar assembly and adhesion to the epithelial host cells. Loss of LuxS/AI-2 signaling diminishes hilD and SPI-1 gene expression, unveiling a regulatory link between quorum sensing and virulence determinants. Further, AI-2 signaling governs resistance to antimicrobial peptides through the pmrD/AB system and supports intracellular proliferation in the host cells. Transcriptomic profiling revealed that LuxS/AI-2 controls distinct gene networks spanning invasion, survival, and immune evasion. In murine infection models, inhibition of LuxS/AI-2 signaling in combination with antibiotics can be an alternative therapeutic approach. Our findings establish LuxS/AI-2 as an integrated regulatory hub in Salmonella pathogenesis and highlight quorum sensing as a targetable mechanism for therapeutic intervention.
Results show that Leptospira meyeri synthesizes N-acyl homoserine lactone family autoinducers, particularly the N-Octanoyl-DL-homoserine lactone family autoinducers, and lay the groundwork for future research on Quorum Sensing systems in Leptospira.
This study provides novel and unexpected insights into the involvement of a LuxR homolog in regulating a QS system in Gram-positive bacteria and demonstrates that functional GBL-based QS systems are conserved and active in R. erythropolis.
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