Species interactions drive the spread of ampicillin resistance in human-associated gut microbiota.
Species interactions drive the spread of ampicillin resistance in human-associated gut microbiota.
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DOI：
10.1093/emph/eoab020
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发表时间：
2021
期刊：
影响因子：
--
通讯作者：
Hall AR
中科院分区：
文献类型：
--
作者：
O'Brien S;Baumgartner M;Hall AR
如果我们要继续成功治疗传染病，减缓抗菌素耐药性的传播就迫在眉睫。越来越多的证据表明，物种之间和物种内部的微生物相互作用是耐药性的重要驱动因素。一方面，耐药基因型的交叉保护可以保护敏感微生物免受抗生素的不利影响，减少耐药性的优势。另一方面，抗生素介导的对易感基因型的杀伤可以减轻竞争，并允许抗性菌株茁壮成长（竞争性释放）。在这里，通过观察从人类采样的微生物群落中的物种内和物种之间的相互作用，我们研究了交叉保护和竞争性释放在驱动氨苄青霉素耐药性在无处不在的肠道寄生虫和机会致病菌大肠杆菌中传播的潜在作用。使用包含嵌入从人类采样的肠道微生物群中的大肠杆菌的厌氧肠道微宇宙，我们测试了响应于临床上重要的β-内酰胺抗生素氨苄青霉素的物种内和物种之间的交叉保护和竞争性释放。虽然在标准实验室条件下（充分混合的LB培养基），交叉保护给了对抗生素敏感的大肠杆菌一个优势，但竞争性释放反而推动了耐药大肠杆菌在肠道微观世界中的传播（氨苄青霉素在敏感菌株存在的情况下促进了耐药细菌的生长）。耐药菌株与肠道微生物群其他成员之间的竞争可以限制氨苄青霉素耐药性的传播。如果抗生素治疗通过杀死敏感菌株来消除与常驻微生物的竞争，那么基于微生物群的干预措施可以恢复竞争，这可能是减缓耐药性传播的关键。减缓全球抗生素耐药性的蔓延是一项紧迫的任务。在本文中，我们询问微生物物种之间的相互作用如何驱动耐药性的传播。我们表明，抗生素杀死易感微生物可以为耐药微生物释放资源，并使它们茁壮成长。因此，我们应该根据微生物的社会相互作用来考虑它们，以了解耐药性的传播。
Slowing the spread of antimicrobial resistance is urgent if we are to continue treating infectious diseases successfully. There is increasing evidence microbial interactions between and within species are significant drivers of resistance. On one hand, cross-protection by resistant genotypes can shelter susceptible microbes from the adverse effects of antibiotics, reducing the advantage of resistance. On the other hand, antibiotic-mediated killing of susceptible genotypes can alleviate competition and allow resistant strains to thrive (competitive release). Here, by observing interactions both within and between species in microbial communities sampled from humans, we investigate the potential role for cross-protection and competitive release in driving the spread of ampicillin resistance in the ubiquitous gut commensal and opportunistic pathogen Escherichia coli. Using anaerobic gut microcosms comprising E.coli embedded within gut microbiota sampled from humans, we tested for cross-protection and competitive release both within and between species in response to the clinically important beta-lactam antibiotic ampicillin. While cross-protection gave an advantage to antibiotic-susceptible E.coli in standard laboratory conditions (well-mixed LB medium), competitive release instead drove the spread of antibiotic-resistant E.coli in gut microcosms (ampicillin boosted growth of resistant bacteria in the presence of susceptible strains). Competition between resistant strains and other members of the gut microbiota can restrict the spread of ampicillin resistance. If antibiotic therapy alleviates competition with resident microbes by killing susceptible strains, as here, microbiota-based interventions that restore competition could be a key for slowing the spread of resistance. Slowing the spread of global antibiotic resistance is an urgent task. In this paper, we ask how interactions between microbial species drive the spread of resistance. We show that antibiotic killing of susceptible microbes can free up resources for resistant microbes and allow them to thrive. Therefore, we should consider microbes in light of their social interactions to understand the spread of resistance.
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影响因子：
6.7
作者：
Huijben S;Bell AS;Sim DG;Tomasello D;Mideo N;Day T;Read AF
通讯作者：
Read AF
DOI：
10.1038/nri3535
发表时间：
2013-11
期刊：
Nature reviews. Immunology
影响因子：
--
作者：
通讯作者：
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影响因子：
8.7
作者：
Kim S;Covington A;Pamer EG
通讯作者：
Pamer EG
DOI：
10.1098/rspb.2004.2916
发表时间：
2005-01-07
影响因子：
4.7
作者：
Dugatkin, LA;Perlin, M;Atlas, R
通讯作者：
Atlas, R
DOI：
10.1038/nrmicro2259
发表时间：
2010-01
期刊：
Nature reviews. Microbiology
影响因子：
--
作者：
通讯作者：
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