Antibiotics in feed induce prophages in swine fecal microbiomes.
Antibiotics in feed induce prophages in swine fecal microbiomes.
复制标题
作者：
Allen HK;Looft T;Bayles DO;Humphrey S;Levine UY;Alt D;Stanton TB
抗生素是提高饲料效率和预防农业动物疾病的一种具有成本效益的工具，但其附带作用的全部范围尚不清楚。抗生素已被证明通过在某些细菌菌株中诱导前噬菌体来介导基因转移;因此，一个附带效应可能是在整个肠道微生物组中诱导前噬菌体。在这里，我们使用宏基因组学来评估饲料中的两种抗生素（卡铂和ASP 250 [金霉素，磺胺二甲嘧啶和青霉素]）对猪肠道噬菌体宏基因组（病毒组）的影响。我们还使用16 S rRNA基因测序监测细菌群落。ASP 250，而不是卡巴斯基，引起了噬菌体和细菌群落的显着人口变化。抗生素耐药基因，如多药耐药外排泵，在病毒组中被确定，但在饲料抗生素引起其丰度没有显着变化。噬菌体整合酶编码基因的丰度显着增加，在病毒组中的药物治疗的猪在病毒组中的nonmedicated猪，证明了诱导与抗生素治疗的原噬菌体。还检查了噬菌体-细菌种群动态。我们观察到，当链球菌（捕食者）丰富时，链球菌细菌（猎物）的相对丰度下降，支持猪粪便微生物组中种群动态的“赢家”生态模型。数据表明，肠道生态系统动力学的影响，前噬菌体诱导是饲料中抗生素的附带影响。这项研究推进了我们对饲料中抗生素的附带影响的认识，当时农业中广泛使用“促生长”抗生素正在受到审查。使用比较宏基因组学，我们表明，原噬菌体是由猪粪便微生物组中的饲料中抗生素诱导的，并且在大多数病毒组中检测到抗生素抗性基因。这表明，饲料中的抗生素有助于噬菌体介导的基因转移，潜在的抗生素耐药基因，在猪肠道。此外，噬菌体-细菌种群动力学的所谓“胜者为赢家”模型已在水生生态系统中得到证实，但在肠道生态系统中却遇到了相互矛盾的证据。这些数据支持了猪粪便链球菌细菌和它们的细菌遵循赢家模型的观点。了解细菌在肠道微生物生态学中的作用是抗生素耐药性问题和开发潜在缓解策略的重要组成部分。
Antibiotics are a cost-effective tool for improving feed efficiency and preventing disease in agricultural animals, but the full scope of their collateral effects is not understood. Antibiotics have been shown to mediate gene transfer by inducing prophages in certain bacterial strains; therefore, one collateral effect could be prophage induction in the gut microbiome at large. Here we used metagenomics to evaluate the effect of two antibiotics in feed (carbadox and ASP250 [chlortetracycline, sulfamethazine, and penicillin]) on swine intestinal phage metagenomes (viromes). We also monitored the bacterial communities using 16S rRNA gene sequencing. ASP250, but not carbadox, caused significant population shifts in both the phage and bacterial communities. Antibiotic resistance genes, such as multidrug resistance efflux pumps, were identified in the viromes, but in-feed antibiotics caused no significant changes in their abundance. The abundance of phage integrase-encoding genes was significantly increased in the viromes of medicated swine over that in the viromes of nonmedicated swine, demonstrating the induction of prophages with antibiotic treatment. Phage-bacterium population dynamics were also examined. We observed a decrease in the relative abundance of Streptococcus bacteria (prey) when Streptococcus phages (predators) were abundant, supporting the “kill-the-winner” ecological model of population dynamics in the swine fecal microbiome. The data show that gut ecosystem dynamics are influenced by phages and that prophage induction is a collateral effect of in-feed antibiotics. This study advances our knowledge of the collateral effects of in-feed antibiotics at a time in which the widespread use of “growth-promoting” antibiotics in agriculture is under scrutiny. Using comparative metagenomics, we show that prophages are induced by in-feed antibiotics in swine fecal microbiomes and that antibiotic resistance genes were detected in most viromes. This suggests that in-feed antibiotics are contributing to phage-mediated gene transfer, potentially of antibiotic resistance genes, in the swine gut. Additionally, the so-called “kill-the-winner” model of phage-bacterium population dynamics has been shown in aquatic ecosystems but met with conflicting evidence in gut ecosystems. The data support the idea that swine fecal Streptococcus bacteria and their phages follow the kill-the-winner model. Understanding the role of phages in gut microbial ecology is an essential component of the antibiotic resistance problem and of developing potential mitigation strategies.