在金黄色葡萄球菌中，σ因子sigB的过表达赋予了对CSαβ型抗菌肽ASABF-α的体外抗性。

In vitro resistance to the CSalphabeta-type antimicrobial peptide ASABF-alpha is conferred by overexpression of sigma factor sigB in Staphylococcus aureus.

作者信息

Zhang Hong, Morikawa Kazuya, Ohta Toshiko, Kato Yusuke

机构信息

Department of Developmental Biology, National Institute of Agrobiological Sciences, Oowashi 1-2, Tsukuba, Ibaraki 305-8634, Japan.

出版信息

J Antimicrob Chemother. 2005 May;55(5):686-91. doi: 10.1093/jac/dki070. Epub 2005 Mar 10.

DOI:10.1093/jac/dki070

PMID:15761069

Abstract

OBJECTIVES

ASABF (Ascaris suum antibacterial factor) is a CSalphabeta-type antimicrobial peptide isolated from nematodes. ASABF-alpha, a member of ASABF, is particularly effective against the gram-positive pathogen Staphylococcus aureus. In this study, we investigated the role of sigB expression on ASABF-resistance in S. aureus.

METHODS

Based on preliminary characterization of the ASABF-resistant strain, Mu50, we speculated that the alternative sigma factor sigB may regulate resistance against antimicrobial peptides. To test this hypothesis, the ASABF susceptibility was compared between NKSB (a sigB-knockout derivative of N315) and its sigB-overexpressing derivative. In addition, similar experiments were carried out for N315ex, a deletion mutant of N315 for SCCmec (Staphylococcus cassette chromosome mec) which contains essential genes for beta-lactam resistance.

RESULTS

The sigB-overexpressing NKSB acquired an increased resistance to ASABF-alpha compared with the parent strain. The sigB-induced ASABF-alpha resistance was also observed in N315ex.

CONCLUSIONS

The overexpression of sigB confers resistance to the antimicrobial peptide, ASABF-alpha. SCCmec is not essential for this resistance.

摘要

目的

猪蛔虫抗菌因子（ASABF）是一种从线虫中分离出的CSαβ型抗菌肽。ASABF-α是ASABF的成员之一，对革兰氏阳性病原体金黄色葡萄球菌特别有效。在本研究中，我们调查了sigB表达在金黄色葡萄球菌对ASABF耐药性中的作用。

方法

基于对ASABF耐药菌株Mu50的初步表征，我们推测替代σ因子sigB可能调节对抗菌肽的耐药性。为了验证这一假设，比较了NKSB（N315的sigB基因敲除衍生物）与其sigB过表达衍生物对ASABF的敏感性。此外，对N315ex进行了类似实验，N315ex是N315的SCCmec（葡萄球菌盒式染色体mec）缺失突变体，其中包含β-内酰胺耐药性的必需基因。