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金黄色葡萄球菌通过磷壁酸的 D-丙氨酸化来颠覆皮肤防御。

Staphylococcus aureus subverts cutaneous defense by D-alanylation of teichoic acids.

出版信息

Exp Dermatol. 2013 Apr;22(4):294-6. doi: 10.1111/exd.12114.

DOI:10.1111/exd.12114
PMID:23528217
Abstract

The Gram-positive bacterium Staphylococcus aureus is a frequent skin colonizer that often causes severe skin infections. It has been reported that neutralizing the negatively charged bacterial surface through the incorporation of d-alanine in its teichoic acids confers reduced susceptibility of S. aureus towards cationic antimicrobial peptides (AMPs). Using a S. aureus strain deficient in d-alanylated teichoic acids (dltA mutant), we demonstrate that d-alanylation of its surface reduces the susceptibility of S. aureus to skin-derived AMPs such as RNase 7 and human beta-defensins. This is accompanied by a higher killing activity of skin extracts towards the S. aureus dltA mutant as well as towards clinical isolates expressing lower levels of dltA. We conclude that modulation of cell envelope d-alanylation may help S. aureus to persist on human skin through evasion of cutaneous innate defense provided by cationic skin-derived AMPs.

摘要

革兰氏阳性菌金黄色葡萄球菌是一种常见的皮肤定植菌,常引起严重的皮肤感染。据报道,通过在其磷壁酸中掺入 D-丙氨酸来中和带负电荷的细菌表面,可降低金黄色葡萄球菌对阳离子抗菌肽 (AMP) 的敏感性。我们使用一种缺乏 D-丙氨酰化磷壁酸的金黄色葡萄球菌 (dltA 突变体) 菌株证明,其表面的 D-丙氨酰化降低了金黄色葡萄球菌对皮肤来源的 AMP(如 RNase 7 和人 β-防御素)的敏感性。这伴随着皮肤提取物对金黄色葡萄球菌 dltA 突变体以及表达较低水平 dltA 的临床分离株的更高杀伤活性。我们得出结论,细胞包膜 D-丙氨酰化的调节可能有助于金黄色葡萄球菌通过逃避阳离子皮肤来源的 AMP 提供的皮肤先天防御来在人体皮肤上持续存在。

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