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Increased resistance of a methicillin-resistant Staphylococcus aureus Δagr mutant with modified control in fatty acid metabolism.
AMB Express ( IF 3.7 ) Pub Date : 2020-04-07 , DOI: 10.1186/s13568-020-01000-y
Hun-Suk Song 1 , Tae-Rim Choi 1 , Yeong-Hoon Han 1 , Ye-Lim Park 1 , Jun Young Park 1 , Soo-Yeon Yang 1 , Shashi Kant Bhatia 1, 2 , Ranjit Gurav 1 , Yun-Gon Kim 3 , Jae-Seok Kim 4 , Hwang-Soo Joo 5 , Yung-Hun Yang 1, 2
Affiliation  

Methicillin-resistant Staphylococcus aureus (MRSA) strains are distinct from general Staphylococcus strains with respect to the composition of the membrane, ability to form a thicker biofilm, and, importantly, ability to modify the target of antibiotics to evade their activity. The agr gene is an accessory global regulator of gram-positive bacteria that governs virulence or resistant mechanisms and therefore an important target for the control of resistant strains. However, the mechanism by which agr impacts resistance to β-lactam antibiotics remains unclear. In the present study, we found the Δagr mutant strain having higher resistance to high concentrations of β-lactam antibiotics such as oxacillin and ampicillin. To determine the influence of variation in the microenvironment of cells between the parental and mutant strains, fatty acid analysis of the supernatant, total lipids, and phospholipid fatty acids were compared. The Δagr mutant strain tended to produce fewer fatty acids and retained lower amounts of C16, C18 fatty acids in the supernatant. Phospholipid analysis showed a dramatic increase in the hydrophobic longer-chain fatty acids in the membrane. To target membrane, we applied several surfactants and found that sorbitan monolaurate (Span20) had a synergistic effect with oxacillin by decreasing biofilm formation and growth. These findings indicate that agr deletion allows for MRSA to resist antibiotics via several changes including constant expression of mecA, fatty acid metabolism, and biofilm thickening.

中文翻译:

甲氧西林抗性金黄色葡萄球菌Δagr突变体的抗药性增强,在脂肪酸代谢中的控制得到了改进。

耐甲氧西林金黄色葡萄球菌(MRSA)菌株与一般葡萄球菌菌株的区别在于其膜的成分,形成较厚的生物膜的能力以及重要的是修饰抗生素靶标以逃避其活性的能力。agr基因是控制毒力或耐药机制的革兰氏阳性细菌的辅助全局调节剂,因此是控制耐药菌株的重要靶标。但是,农杆菌对β-内酰胺类抗生素产生抗药性的机制仍不清楚。在本研究中,我们发现Δagr突变株对高浓度的β-内酰胺类抗生素(例如奥沙西林和氨苄青霉素)具有较高的抗性。为了确定亲本和突变菌株之间细胞微环境变化的影响,比较上清液的脂肪酸分析,总脂质和磷脂脂肪酸。Δagr突变株倾向于产生较少的脂肪酸,并在上清液中保留较少量的C16,C18脂肪酸。磷脂分析表明,膜中的疏水性长链脂肪酸急剧增加。为了靶向膜,我们应用了几种表面活性剂,发现脱水山梨糖醇单月桂酸酯(Span20)通过减少生物膜的形成和生长与奥沙西林具有协同作用。这些发现表明,agr缺失使MRSA通过多种变化(包括mecA的恒定表达,脂肪酸代谢和生物膜增厚)抵抗抗生素。Δagr突变株倾向于产生较少的脂肪酸,并在上清液中保留较少量的C16,C18脂肪酸。磷脂分析表明,膜中的疏水性长链脂肪酸急剧增加。为了靶向膜,我们应用了几种表面活性剂,发现脱水山梨糖醇单月桂酸酯(Span20)通过减少生物膜的形成和生长与奥沙西林具有协同作用。这些发现表明,agr缺失使MRSA通过多种变化(包括mecA的恒定表达,脂肪酸代谢和生物膜增厚)抵抗抗生素。Δagr突变株倾向于产生较少的脂肪酸,并在上清液中保留较少量的C16,C18脂肪酸。磷脂分析表明,膜中的疏水性长链脂肪酸急剧增加。为了靶向膜,我们应用了几种表面活性剂,发现脱水山梨糖醇单月桂酸酯(Span20)通过减少生物膜的形成和生长与奥沙西林具有协同作用。这些发现表明,agr缺失使MRSA通过多种变化(包括mecA的恒定表达,脂肪酸代谢和生物膜增厚)抵抗抗生素。我们应用了几种表面活性剂,发现脱水山梨糖醇单月桂酸酯(Span20)通过减少生物膜的形成和生长与奥沙西林具有协同作用。这些发现表明,agr缺失使MRSA通过多种变化(包括mecA的恒定表达,脂肪酸代谢和生物膜增厚)抵抗抗生素。我们应用了几种表面活性剂,发现脱水山梨糖醇单月桂酸酯(Span20)通过减少生物膜的形成和生长与奥沙西林具有协同作用。这些发现表明,agr缺失使MRSA通过多种变化(包括mecA的恒定表达,脂肪酸代谢和生物膜增厚)抵抗抗生素。
更新日期:2020-04-20
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