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Gene Regulation in Microbial Communities: Quorum Sensing01:28

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Quorum sensing is a mechanism of bacterial communication that enables coordinated gene expression in response to changes in population density. This facilitates collective behaviors that enhance survival, resource acquisition, and ecological adaptation. This process relies on small signaling molecules called autoinducers that accumulate as bacterial populations grow. When a critical threshold concentration of autoinducers is reached, bacterial cells collectively modify gene expression,...
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Bacterial signaling can occur within bacteria (intracellular) or between bacteria (intercellular). At times, a group of bacteria behaves like a community. To achieve this, they engage in quorum sensing, the perception of higher cell density that causes changes in gene expression. Quorum sensing involves both extracellular and intracellular signaling. The signaling cascade starts with a molecule called an autoinducer (AI). Individual bacteria produce AIs that move out of the bacterial cell...
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Anti-virulent Disruption of Pathogenic Biofilms using Engineered Quorum-quenching Lactonases
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Molecular Communication-Based Quorum Sensing Disruption for Enhanced Immune Defense.

Shees Zulfiqar, Ozgur B Akan

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    This summary is machine-generated.

    Molecular Communication (MC) disrupts bacterial Quorum Sensing (QS) pathways to enhance immune defense against resistant bacteria. This approach, using RNAIII-inhibitor (RIP), reduces virulence and boosts the immune system, aiding in fighting infections.

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    Area of Science:

    • Biochemistry
    • Microbiology
    • Immunology

    Background:

    • Bacteria utilize Quorum Sensing (QS) to coordinate virulence and antibiotic resistance.
    • Antimicrobial resistance poses a significant global health threat.
    • Molecular Communication (MC) offers novel strategies for pharmaceutical interventions.

    Purpose of the Study:

    • To explore an MC-based approach to disrupt bacterial QS pathways.
    • To enhance immune defenses against antimicrobial-resistant bacteria.
    • To investigate the efficacy of RNAIII-inhibitor (RIP) in Staphylococcus aureus.

    Main Methods:

    • Interfering with bacterial autoinducer signaling pathways.
    • Utilizing RNAIII-inhibitor (RIP) to block key transcript synthesis in the Accessory Gene Regulator (AGR) system.
    • Evaluating the synergistic effects of QS inhibitors with conventional antimicrobials.

    Main Results:

    • Disruption of QS pathways cripples bacterial virulence and resistance mechanisms.
    • RIP effectively blocks RNAII and RNAIII synthesis, reducing toxin production and immune evasion.
    • Combination therapy with QS inhibitors and antimicrobials lowers required antibiotic doses and reduces resistance pressure.

    Conclusions:

    • MC-based strategies can effectively target bacterial communication to combat infections.
    • This approach bolsters host immune responses against pathogens.
    • MC offers a promising avenue for managing drug-resistant bacterial infections.