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<p>Antibiotic resistance genes (ARGs), which spread via horizontal gene transfer, pose a significant threat to global health. Although exogenous stressors are known to promote conjugation, the role of endogenous microbial metabolites remains poorly understood. Here we report that hydrogen sulfide (H<sub>2</sub>S)—a ubiquitous metabolite in wastewater—acts as a potent, yet overlooked, promoter of plasmid conjugation, enhancing conjugation frequency and broadening the recipient range of plasmid RP4 within wastewater microbiota. We elucidate a plasmid-autonomous activation mechanism distinct from the classic SOS response. Specifically, plasmid RP4 uses its encoded protein Upf32.8 (renamed GlsS32.8) to sense intracellular glutamine levels, trigger plasmid de-repression and enhance RP4-specific glutamine-centric metabolic hijacking from the host, thereby facilitating conjugation under H<sub>2</sub>S. Notably, evolutionary analysis shows that GlsS32.8 is conserved across globally prevalent IncP-1α plasmids, underscoring a universal risk of ARG spread in H<sub>2</sub>S-rich environments. Our findings redefine microbial metabolites as critical players in resistance spread and provide valuable insights into plasmid–host interactions for combatting ARG dissemination.</p>

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Hydrogen sulfide drives horizontal transfer of plasmid-borne antibiotic resistance genes in wastewater ecosystems

  • 期刊论文

  • 发表日期：

    2025年11月7日

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  • Haining Huang,
  • Lin Lin,
  • Qimeng Liu,
  • Xinyi Li,
  • Junqi Liao,
  • Lei Dong,
  • Junya Zhang,
  • Yinglong Su,
  • Jingyang Luo,
  • Leiyu Feng,
  • Xiong Zheng,
  • Jianhua Guo,
  • Yinguang Chen

摘要

Antibiotic resistance genes (ARGs), which spread via horizontal gene transfer, pose a significant threat to global health. Although exogenous stressors are known to promote conjugation, the role of endogenous microbial metabolites remains poorly understood. Here we report that hydrogen sulfide (H2S)—a ubiquitous metabolite in wastewater—acts as a potent, yet overlooked, promoter of plasmid conjugation, enhancing conjugation frequency and broadening the recipient range of plasmid RP4 within wastewater microbiota. We elucidate a plasmid-autonomous activation mechanism distinct from the classic SOS response. Specifically, plasmid RP4 uses its encoded protein Upf32.8 (renamed GlsS32.8) to sense intracellular glutamine levels, trigger plasmid de-repression and enhance RP4-specific glutamine-centric metabolic hijacking from the host, thereby facilitating conjugation under H2S. Notably, evolutionary analysis shows that GlsS32.8 is conserved across globally prevalent IncP-1α plasmids, underscoring a universal risk of ARG spread in H2S-rich environments. Our findings redefine microbial metabolites as critical players in resistance spread and provide valuable insights into plasmid–host interactions for combatting ARG dissemination.