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<p><i>Cronobacter sakazakii</i> is an important neonatal pathogen frequently associated with powdered infant formula. However, the mechanisms by which <i>C. sakazakii</i> adapts to the host environment and establishes systemic dissemination remain poorly understood. Here, we reveal a signal transduction pathway centered on a novel sRNA, CsrN, which facilitates <i>C. sakazakii</i> in utilizing nitrate respiration in response to oxygen-limited environments within the host, thereby enhancing its virulence in vivo. <i>C. sakazakii</i> infection triggers an inflammatory response, leading to the accumulation of host-derived nitrate, a key alternative electron acceptor. The expression of CsrN is induced under anaerobic conditions via the ArcAB two-component regulation system. CsrN subsequently enhances the expression of the <i>narGHJI</i> operon, which encodes a nitrate reductase complex. This promotes the colonization of <i>C. sakazakii</i> in the gastrointestinal tract and benefits its survival within macrophages, ultimately leading to increased systemic bacterial dissemination and virulence in the host. We show that administration of tungstate, a specific inhibitor of nitrate respiration, significantly attenuates <i>C. sakazakii</i> virulence in animal experiments. This work provides novel insights into the survival and pathogenicity mechanisms employed by <i>C. sakazakii</i> in host environments and suggests nitrate respiration as a potential therapeutic target for combating <i>C. sakazakii</i> infections.</p>

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sRNA centered signaling activates nitrate respiration and enhances Cronobacter sakazakii virulence in host environments

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年3月3日

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  • Xiaoya Li,
  • Hao Sun,
  • Xinyuan Yang,
  • Liying Feng,
  • Yuanyuan Niu,
  • Binbin Xiang,
  • Jingliang Qin,
  • Jiake Wang,
  • Zhengang Li,
  • Lu Wang,
  • Lu Feng,
  • Lei Wang,
  • Bin Liu

摘要

Cronobacter sakazakii is an important neonatal pathogen frequently associated with powdered infant formula. However, the mechanisms by which C. sakazakii adapts to the host environment and establishes systemic dissemination remain poorly understood. Here, we reveal a signal transduction pathway centered on a novel sRNA, CsrN, which facilitates C. sakazakii in utilizing nitrate respiration in response to oxygen-limited environments within the host, thereby enhancing its virulence in vivo. C. sakazakii infection triggers an inflammatory response, leading to the accumulation of host-derived nitrate, a key alternative electron acceptor. The expression of CsrN is induced under anaerobic conditions via the ArcAB two-component regulation system. CsrN subsequently enhances the expression of the narGHJI operon, which encodes a nitrate reductase complex. This promotes the colonization of C. sakazakii in the gastrointestinal tract and benefits its survival within macrophages, ultimately leading to increased systemic bacterial dissemination and virulence in the host. We show that administration of tungstate, a specific inhibitor of nitrate respiration, significantly attenuates C. sakazakii virulence in animal experiments. This work provides novel insights into the survival and pathogenicity mechanisms employed by C. sakazakii in host environments and suggests nitrate respiration as a potential therapeutic target for combating C. sakazakii infections.