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首页> 美国卫生研究院文献>Antimicrobial Agents and Chemotherapy >Effects of Amoxicillin Gentamicin and Moxifloxacin on the Hemolytic Activity of Staphylococcus aureus In Vitro and In Vivo
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Effects of Amoxicillin Gentamicin and Moxifloxacin on the Hemolytic Activity of Staphylococcus aureus In Vitro and In Vivo

机译：阿莫西林庆大霉素和莫西沙星对金黄色葡萄球菌体内外溶血活性的影响

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In Staphylococcus aureus infection hemolysis caused by the extracellular protein α-toxin encoded by hla is thought to contribute significantly to its multifactorial virulence. In vitro, subinhibitory concentrations of β-lactam antibiotics and fluoroquinolones increase the levels of hla and α-toxin expression, whereas aminoglycosides decrease the levels of hla and α-toxin expression. In the present study we investigated the effects of subinhibitory concentrations of amoxicillin, gentamicin, and moxifloxacin on hla and α-toxin expression and total hemolysis of S. aureus strain 8325-4, a high-level α-toxin producer, and its α-toxin-negative mutant, DU 1090, in vitro and in a rat model of chronic S. aureus infection. The levels of expression of hla and α-toxin and total hemolysis did not differ significantly when amoxicillin, gentamicin, or moxifloxacin was added to cultures of S. aureus strain 8325-4. In vivo, strain 8325-4 induced a significantly increased level of hemolysis in infected pouches compared to that in uninfected control pouches, but the hemolysis was reduced to control levels by treatment with doses of amoxicillin, gentamicin, or moxifloxacin that reduced bacterial numbers by 2 orders of magnitude. Additionally, the effects of subinhibitory concentrations of the three antibiotics on total hemolysis of four methicillin-resistant S. aureus and three methicillin-sensitive S. aureus (MSSA) clinical isolates were assessed in vitro. A significant increase in total hemolysis was observed for only one MSSA strain when it was treated with amoxicillin but not when it was treated with moxifloxacin or gentamicin. When purified α-toxin was incubated with purified human neutrophil elastase, α-toxin was cleaved nearly completely. The results suggest that the penicillin-induced increases in S. aureus α-toxin expression are strain dependent, that reduction of bacterial numbers in vivo counteracts this phenomenon effectively, and finally, that in localized S. aureus infections α-toxin activity is controlled by neutrophil elastase.
机译：在金黄色葡萄球菌感染中，由hla编码的细胞外蛋白α毒素引起的溶血被认为是对其多因素毒力的重要贡献。在体外，亚抑菌浓度的β-内酰胺类抗生素和氟喹诺酮类药物会增加hla和α-毒素表达水平，而氨基糖苷会降低hla和α-毒素表达水平。在本研究中，我们研究了亚抑制浓度的阿莫西林，庆大霉素和莫西沙星对高水平α毒素产生者金黄色葡萄球菌8325-4株及其α-毒素的hla和α-毒素表达以及总溶血的影响。毒素阴性突变体DU 1090，在体外和慢性金黄色葡萄球菌感染的大鼠模型中。向金黄色葡萄球菌8325-4菌株中加入阿莫西林，庆大霉素或莫西沙星后，hla和α-毒素的表达水平及总溶血度无明显差异。在体内，与未感染的对照袋相比，菌株8325-4诱导的被感染袋中的溶血水平显着增加，但是通过使用阿莫西林，庆大霉素或莫西沙星的剂量处理可使溶血量降低至对照水平，细菌数量减少了2数量级。另外，在体外评估了三种抗生素亚抑制浓度对四种耐甲氧西林金黄色葡萄球菌和三种耐甲氧西林金黄色葡萄球菌（MSSA）临床分离株的总溶血作用。当用阿莫西林治疗时，仅一种MSSA菌株观察到总溶血显着增加，而当用莫西沙星或庆大霉素治疗时则未观察到。当将纯化的α-毒素与纯化的人嗜中性粒细胞弹性蛋白酶温育时，α-毒素几乎被完全裂解。结果表明，青霉素诱导的金黄色葡萄球菌α-毒素表达增加是菌株依赖性的，体内细菌数量的减少有效地抵消了这种现象，最后，在局部金黄色葡萄球菌感染中α-毒素的活性受以下因素控制：中性粒细胞弹性蛋白酶。

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