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Beta-lactam-Induced Outer Membrane Alteration Confers E. coli a Fortuitous Competitive Advantage through Cross-Resistance to Bacteriophages
Environmental Science & Technology Letters ( IF 8.9 ) Pub Date : 2020-04-22 , DOI: 10.1021/acs.estlett.0c00318 Pengxiao Zuo 1 , Pingfeng Yu 1 , Pedro J. J. Alvarez 1
Environmental Science & Technology Letters ( IF 8.9 ) Pub Date : 2020-04-22 , DOI: 10.1021/acs.estlett.0c00318 Pengxiao Zuo 1 , Pingfeng Yu 1 , Pedro J. J. Alvarez 1
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Bacteriophages play an important role in controlling bacteria populations; yet, little is known about their differential effects on antibiotic resistant bacteria (ARB) proliferation. Here, we report that beta-lactam resistance may fortuitously confer phage resistance as a critical factor for enhanced ARB proliferation. Following sublethal exposure to amoxicillin, Escherichia coli experienced lipopolysaccharides (LPS) modifications (corroborated by FTIR) and became cross-resistant to various phages that adsorb to receptors on LPS as the first infection step. Although, wildtype cells’ LPS adsorbed 39 ± 8.7% of T3 phages, cross-resistant cells’ LPS only adsorbed 4.1 ± 2.3%. We demonstrate the relevance of this phenomenon using activated sludge microcosms. Cross-resistant E. coli experienced a negligible decrease from 6.27 ± 0.07 to 6.07 ± 0.18 log CFU/mL after 5 days, whereas the wildtype decayed from 6.11 ± 0.13 to 5.29 ± 0.02 log CFU/mL. Furthermore, cross-resistant E. coli (but not wildtype) proliferated in Luria broth-fed microcosms. We also show a fitness cost associated with amoxicillin resistance; however, due to acquired phage resistance, cross-resistant E. coli had greater fitness than the wildtype. Overall, this study demonstrates that antibiotics can alter interactions between phages and bacteria, resulting in an overlooked competitive advantage for antibiotic-resistance propagation.
中文翻译：
β-内酰胺诱导的外膜改变通过对噬菌体的交叉耐药性赋予了大肠杆菌以偶然的竞争优势。
噬菌体在控制细菌种群中起着重要作用。然而，关于它们对抗生素抗性细菌（ARB）增殖的不同影响知之甚少。在这里，我们报告说，β-内酰胺抗性可能偶然地将噬菌体抗性作为增强ARB增殖的关键因素。亚致死性暴露于阿莫西林后，大肠杆菌经历了脂多糖（LPS）修饰（由FTIR证实），并且对吸收到LPS受体的各种噬菌体产生交叉耐药性，这是第一步感染。尽管野生型细胞的LPS吸附了39±8.7％的T3噬菌体，但交叉耐药细胞的LPS仅吸附了4.1±2.3％。我们证明了使用活性污泥微观世界这种现象的相关性。交叉耐药大肠杆菌5天后从6.27±0.07下降至6.07±0.18 log CFU / mL可以忽略不计，而野生型从6.11±0.13下降至5.29±0.02 log CFU / mL。此外，交叉抗性大肠杆菌（但不是野生型）在Luria肉汤喂养的微观世界中增殖。我们还显示了与阿莫西林耐药性相关的健身成本；然而，由于获得的噬菌体抗性，交叉抗性的大肠杆菌比野生型具有更大的适应性。总体而言，这项研究表明，抗生素可以改变噬菌体与细菌之间的相互作用，从而导致抗生素耐药性传播的竞争优势被忽略。
更新日期：2020-04-22
中文翻译：
β-内酰胺诱导的外膜改变通过对噬菌体的交叉耐药性赋予了大肠杆菌以偶然的竞争优势。
噬菌体在控制细菌种群中起着重要作用。然而，关于它们对抗生素抗性细菌（ARB）增殖的不同影响知之甚少。在这里，我们报告说，β-内酰胺抗性可能偶然地将噬菌体抗性作为增强ARB增殖的关键因素。亚致死性暴露于阿莫西林后，大肠杆菌经历了脂多糖（LPS）修饰（由FTIR证实），并且对吸收到LPS受体的各种噬菌体产生交叉耐药性，这是第一步感染。尽管野生型细胞的LPS吸附了39±8.7％的T3噬菌体，但交叉耐药细胞的LPS仅吸附了4.1±2.3％。我们证明了使用活性污泥微观世界这种现象的相关性。交叉耐药大肠杆菌5天后从6.27±0.07下降至6.07±0.18 log CFU / mL可以忽略不计，而野生型从6.11±0.13下降至5.29±0.02 log CFU / mL。此外，交叉抗性大肠杆菌（但不是野生型）在Luria肉汤喂养的微观世界中增殖。我们还显示了与阿莫西林耐药性相关的健身成本；然而，由于获得的噬菌体抗性，交叉抗性的大肠杆菌比野生型具有更大的适应性。总体而言，这项研究表明，抗生素可以改变噬菌体与细菌之间的相互作用，从而导致抗生素耐药性传播的竞争优势被忽略。
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