Chatzigiannidou Ioanna, Johansen Pi L, Dehli Rasmus K, Moll Janne Marie, Eriksen Carsten, Myers Pernille N, Roager Henrik M, Yang Lili, Stokholm Jakob, Sørensen Søren J, Krogfelt Karen A, Laursen Martin F, Trivedi Urvish, Scheynius Annika, Kristiansen Karsten, Mie Axel, Alm Johan, Brix Susanne
Department of Biotechnology and Biomedicine, Technical University of Denmark, Kgs. Lyngby, Denmark.
Department of Nutrition, Exercise and Sports, University of Copenhagen, Frederiksberg C, Denmark.
Nat Commun. 2025 Aug 30;16(1):8139. doi: 10.1038/s41467-025-63401-6.
Despite the critical role of the gut resistome in spreading of antimicrobial resistance (AMR), strategies to reduce the abundance of antibiotic resistance genes (ARGs) during microbiota development in infancy remain underexplored. Using longitudinal quantitative metagenomic data, we here show that ARGs are present in the gut microbiota from the first week of life, with a peak in absolute ARG abundance and richness at 6 months. Delivery mode significantly affects early ARG dynamics, and vaginally delivered infants exhibit higher ARG abundance due to maternal transmission of Escherichia coli strains harbouring extensive resistance repertoires. The abundance of E. coli and other ARG-rich taxa inversely correlates with aromatic lactic acid-producing bifidobacteria, and aromatic lactic acids strongly inhibit the in vitro growth of E. coli and other opportunistic ARG-rich taxa. Our results highlight temporal and critical microbial interactions shaping the gut resistome in early infancy, pointing to potential interventions to curb AMR during this vulnerable developmental window by promoting colonization of aromatic lactic acid-producing bifidobacteria.
尽管肠道耐药组在抗生素耐药性(AMR)传播中起关键作用,但在婴儿期微生物群发育过程中减少抗生素抗性基因(ARG)丰度的策略仍未得到充分探索。利用纵向定量宏基因组数据,我们在此表明,ARG在生命的第一周就存在于肠道微生物群中,在6个月时绝对ARG丰度和丰富度达到峰值。分娩方式显著影响早期ARG动态,由于携带广泛耐药谱的大肠杆菌菌株的母体传播,阴道分娩的婴儿表现出更高的ARG丰度。大肠杆菌和其他富含ARG的分类群的丰度与产生芳香族乳酸的双歧杆菌呈负相关,并且芳香族乳酸强烈抑制大肠杆菌和其他富含ARG的机会性分类群的体外生长。我们的结果突出了在婴儿早期塑造肠道耐药组的时间性和关键微生物相互作用,指出了通过促进产生芳香族乳酸的双歧杆菌定殖来在这个脆弱的发育窗口抑制AMR的潜在干预措施。
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