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首页> 外文期刊>Infection and immunity >Staphylococcus aureus Susceptibility to Innate Antimicrobial Peptides, β-Defensins and CAP18, Expressed by Human Keratinocytes
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Staphylococcus aureus Susceptibility to Innate Antimicrobial Peptides, β-Defensins and CAP18, Expressed by Human Keratinocytes

机译：金黄色葡萄球菌对人角质形成细胞表达的天然抗菌肽，β-防御素和CAP18的敏感性

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The antimicrobial peptides human β-defensin-1 (hBD1), hBD2, hBD3, and CAP18 expressed by keratinocytes have been implicated in mediation of the innate defense against bacterial infection. To gain insight into Staphylococcus aureus infection, the susceptibility of S. aureus, including methicillin-resistant S. aureus (MRSA), to these antimicrobial peptides was examined. Based on quantitative PCR, expression of hBD2 mRNA by human keratinocytes was significantly induced by contact with S. aureus, and expression of hBD3 and CAP18 mRNA was slightly induced, while hBD1 mRNA was constitutively expressed irrespective of the presence of S. aureus. Ten clinical S. aureus isolates, including five MRSA isolates, induced various levels of expression of hBD2, hBD3, and CAP18 mRNA by human kertinocytes. The activities of hBD3 and CAP18 against S. aureus were found to be greater than those of hBD1 and hBD2. A total of 44 S. aureus clinical isolates, including 22 MRSA strains, were tested for susceptibility to hBD3 and CAP18. Twelve (55%) and 13 (59%) of the MRSA strains exhibited more than 20% survival in the presence of hBD3 (1 μg/ml) and CAP18 (0.5 μg/ml), respectively. However, only three (13%) and two (9%) of the methicillin-sensitive S. aureus isolates exhibited more than 20% survival with hBD3 and CAP18, respectively, suggesting that MRSA is more resistant to these peptides. A synergistic antimicrobial effect between suboptimal doses of methicillin and either hBD3 or CAP18 was observed with 10 MRSA strains. Furthermore, of several genes associated with methicillin resistance, inactivation of the fmtC gene in MRSA strain COL increased susceptibility to the antimicrobial effect mediated by hBD3 or CAP18.
机译：角质形成细胞表达的抗菌肽人β-防御素1（hBD1），hBD2，hBD3和CAP18参与了抵抗细菌感染的先天防御。为了了解金黄色葡萄球菌感染， S的易感性。金黄色，包括耐甲氧西林的 S。金黄色葡萄球菌（MRSA）对这些抗菌肽的检查。基于定量PCR，与 S接触可显着诱导人角质形成细胞中hBD2 mRNA的表达。无论是否存在 S，hBD3和CAP18 mRNA的表达均被轻微诱导，而hBD1 mRNA的组成型表达则有所不同。金黄色。十个临床 S。金黄色葡萄球菌（包括5种MRSA分离物）可诱导人角质形成细胞表达不同水平的hBD2，hBD3和CAP18 mRNA。 hBD3和CAP18对 S的活性。发现金黄色葡萄球菌大于hBD1和hBD2。总共44个 S。测试了包括22个MRSA菌株在内的金黄色葡萄球菌临床分离株对hBD3和CAP18的敏感性。在存在hBD3（1μg/ ml）和CAP18（0.5μg/ ml）的情况下，十二个（55％）和13（59％）的MRSA菌株显示出超过20％的存活率。但是，对甲氧西林敏感的 S只有3个（13％）和2个（9％）。金黄色葡萄球菌对hBD3和CAP18的存活率分别超过20％，这表明MRSA对这些肽的耐药性更高。用10个MRSA菌株观察到亚最佳剂量的甲氧西林与hBD3或CAP18之间的协同抗菌作用。此外，在几个与甲氧西林抗性相关的基因中，MRSA菌株COL中的 fmtC 基因失活增加了对hBD3或CAP18介导的抗菌作用的敏感性。

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