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Related Concept Videos

Gene Regulation in Microbial Communities: Quorum Sensing01:28

Gene Regulation in Microbial Communities: Quorum Sensing

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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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Methicillin-resistant Staphylococcus aureus (MRSA) presents a critical public health threat, arising from its capacity to resist β-lactam antibiotics due to acquisition of the mecA gene within the staphylococcal cassette chromosome mec (SCCmec). This gene encodes penicillin-binding protein 2a (PBP2a), which impairs binding efficacy of methicillin and other β-lactams. MRSA has evolved into distinct clonal lineages impacting humans and animals alike, reinforcing its significance within...
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Pathogenic bacteria employ a range of regulatory mechanisms to modulate the expression of virulence genes in response to environmental and host-derived signals. These mechanisms ensure that virulence factors are expressed only under favorable conditions, thereby optimizing infection and survival strategies.Mechanisms of Virulence RegulationKey regulatory strategies include:Two-Component Systems: These consist of a membrane-bound sensor kinase and a cytoplasmic response regulator. Environmental...
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An inflammatory response is a localized, nonspecific immune reaction that occurs when a tissue is injured. It is characterized by redness, swelling, heat, and pain, which are commonly called the cardinal signs and symptoms of inflammation. Inflammation can sometimes result in a loss of function.
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Staphylococcus aureus is a Gram-positive coccus that resides harmlessly on the skin and mucous membranes of healthy individuals. When the skin barrier is breached, it can shift from a commensal to an opportunistic pathogen. This transition is facilitated by surface adhesins, such as clumping factor B and S. aureus surface protein G (SasG), which bind to structural proteins, including loricrin and cytokeratin, in the damaged epidermis. Protein A, another key factor, binds the Fc region of...
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ω-Hydroxyemodin limits staphylococcus aureus quorum sensing-mediated pathogenesis and inflammation.

Seth M Daly1, Bradley O Elmore1, Jeffrey S Kavanaugh2

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ω-hydroxyemodin (OHM) combats antibiotic-resistant Staphylococcus aureus by disrupting quorum sensing (QS). This virulence inhibitor enhances bacterial clearance and host immune response in skin infections.

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Area of Science:

  • Microbiology
  • Infectious Diseases
  • Pharmacology

Background:

  • Antibiotic-resistant pathogens pose a significant global health challenge.
  • Staphylococcus aureus is a leading cause of skin and soft tissue infections (SSTIs) with increasing resistance.
  • Bacterial virulence inhibitors offer a potential alternative or adjunct to traditional antibiotics.

Purpose of the Study:

  • To investigate ω-hydroxyemodin (OHM) as a suppressor of Staphylococcus aureus quorum sensing (QS).
  • To characterize the mechanism of OHM's anti-virulence activity.
  • To evaluate OHM's efficacy in a preclinical model of S. aureus infection.

Main Methods:

  • Identified OHM from Penicillium restrictum.
  • Assessed OHM's effect on agr-mediated QS in S. aureus at non-toxic concentrations.
  • Determined OHM's direct binding to the AgrA response regulator.
  • Evaluated OHM in a mouse model of S. aureus SSTI.
  • Assessed OHM's impact on bacterial clearance, inflammation, and host immune cell killing.

Main Results:

  • OHM suppressed QS across all four S. aureus agr alleles at subinhibitory concentrations.
  • OHM directly bound AgrA, inhibiting its interaction with the agr P2 promoter.
  • OHM treatment reduced dermonecrosis, enhanced bacterial clearance, and decreased inflammatory cytokines in a mouse SSTI model.
  • OHM improved S. aureus killing by immune cells in vitro in an agr-dependent manner.

Conclusions:

  • OHM effectively disarms Staphylococcus aureus by suppressing QS.
  • OHM bolsters the host innate immune response and mitigates inflammation.
  • OHM represents a promising therapeutic strategy against antibiotic-resistant S. aureus infections.