Abstract
In this study we investigated the antimicrobial activity of magnolol on Staphylococcus aureus. The minimal inhibitory concentrations of magnolol against 31 S. aureus strains ranged from 4–32 μg/mL. In addition, hemolysin assays, Western blotting, and real-time RT-PCR were performed to investigate the effect of magnolol on α-toxin secretion by both methicillin-sensitive S. aureus (MSSA) and methicillin-resistant S. aureus (MRSA). The results indicated that sub-inhibitory concentrations of magnolol dose-dependently inhibited the transcription of hla (the gene encoding α-toxin) in S. aureus, resulting in a reduction of α-toxin secretion and, thus, hemolytic activities.
Highlights
Staphylococcus aureus is a leading cause of nosocomial infections and the pathogen responsible for a variety of diseases associated with significant morbidity and mortality
The growth characteristics of S. aureus American Type Culture Collection (ATCC) 29213 in the presence of magnolol are shown in Figure 2a, wherein we found that 1/16 × Minimal Inhibitory Concentration (MIC), 1/8 × MIC, and 1/4 × MIC of magnolol had little influence on the growth of S. aureus, after 360 min of magnolol treatment, the OD600 nm values were 99.5, 96.9, and 95.8% of the control culture, respectively
Some β-lactams and glycopeptide agents induce the expression of α-toxin, enterotoxins, and toxic shock syndrome toxin 1 (TSST-1) through a stimulatory effect on exoprotein synthesis [16,17], indicating that the symptoms of infections caused by S. aureus may be aggravated when patients are treated with these antibiotics
Summary
Staphylococcus aureus is a leading cause of nosocomial infections and the pathogen responsible for a variety of diseases associated with significant morbidity and mortality. Like other Gram-positive bacteria, the pathogenicity of S. aureus is largely dependent upon extracellular virulence factors, including both secreted and surface proteins [3]. One of the most important extracellular proteins is α-toxin, a pore-forming, soluble 33-kDa protein that is secreted by most S. aureus strains, primarily during the post-exponential phase. The toxin can cause pore formation of a wide range of human cells, including erythrocytes, monocytes, lymphocytes, macrophages, and epithelial cells. It can induce pro-inflammatory changes in mammalian cells. The present study aimed to assess the antimicrobial activity of magnolol on S. aureus and to investigate the effect of subinhibitory concentrations of magnolol on α-toxin expression by both methicillin-sensitive and methicillin-resistant S. aureus
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