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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Antimicrob+Agents+Chemother
2015 ; 59
(4
): 2223-35
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?-Hydroxyemodin limits staphylococcus aureus quorum sensing-mediated pathogenesis
and inflammation
#MMPMID25645827
Daly SM
; Elmore BO
; Kavanaugh JS
; Triplett KD
; Figueroa M
; Raja HA
; El-Elimat T
; Crosby HA
; Femling JK
; Cech NB
; Horswill AR
; Oberlies NH
; Hall PR
Antimicrob Agents Chemother
2015[Apr]; 59
(4
): 2223-35
PMID25645827
show ga
Antibiotic-resistant pathogens are a global health threat. Small molecules that
inhibit bacterial virulence have been suggested as alternatives or adjuncts to
conventional antibiotics, as they may limit pathogenesis and increase bacterial
susceptibility to host killing. Staphylococcus aureus is a major cause of
invasive skin and soft tissue infections (SSTIs) in both the hospital and
community settings, and it is also becoming increasingly antibiotic resistant.
Quorum sensing (QS) mediated by the accessory gene regulator (agr) controls
virulence factor production essential for causing SSTIs. We recently identified
?-hydroxyemodin (OHM), a polyhydroxyanthraquinone isolated from solid-phase
cultures of Penicillium restrictum, as a suppressor of QS and a compound sought
for the further characterization of the mechanism of action. At concentrations
that are nontoxic to eukaryotic cells and subinhibitory to bacterial growth, OHM
prevented agr signaling by all four S. aureus agr alleles. OHM inhibited QS by
direct binding to AgrA, the response regulator encoded by the agr operon,
preventing the interaction of AgrA with the agr P2 promoter. Importantly, OHM was
efficacious in a mouse model of S. aureus SSTI. Decreased dermonecrosis with OHM
treatment was associated with enhanced bacterial clearance and reductions in
inflammatory cytokine transcription and expression at the site of infection.
Furthermore, OHM treatment enhanced the immune cell killing of S. aureus in vitro
in an agr-dependent manner. These data suggest that bacterial disarmament through
the suppression of S. aureus QS may bolster the host innate immune response and
limit inflammation.
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