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<p>Animals integrate internal states to guide survival-critical decisions, but whether and how intestinal bacteria influence this process by interacting with host metabolic cues remains unclear. Here we show that the intestinal pathogen <i>P. aeruginosa</i> overrides host decision-making in fasted <i>C. elegans</i> by modulating central serotonin (5-HT) signaling. Fasting promotes risk-taking by activating an intestinal energy-sensing pathway that induces the chemoreceptor SRI-36 in ADF 5-HT neurons, sensitizing ADF to food odors and triggering moderate 5-HT release that drives food attraction despite risk. In contrast, intestinal <i>P. aeruginosa</i> reverses this strategy by activating a distinct immune-brain axis that further amplifies SRI-36 expression and ADF sensitivity, leading to excessive 5-HT release that suppresses food attraction and prioritizes safety. These findings reveal a gut-to-brain mechanism by which metabolic and immune signals converge on central 5-HT to reshape behavioral strategies.</p>

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Intestinal pathogens override hunger-driven decision-making via immune regulation of central serotonin signaling in C. elegans

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年2月25日

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  • Ying Lei,
  • Chao Chen,
  • Xu Zhan,
  • Mingshu Xie,
  • Ying Wang,
  • Hao Li,
  • Jiale Zhang,
  • Ping Liu

摘要

Animals integrate internal states to guide survival-critical decisions, but whether and how intestinal bacteria influence this process by interacting with host metabolic cues remains unclear. Here we show that the intestinal pathogen P. aeruginosa overrides host decision-making in fasted C. elegans by modulating central serotonin (5-HT) signaling. Fasting promotes risk-taking by activating an intestinal energy-sensing pathway that induces the chemoreceptor SRI-36 in ADF 5-HT neurons, sensitizing ADF to food odors and triggering moderate 5-HT release that drives food attraction despite risk. In contrast, intestinal P. aeruginosa reverses this strategy by activating a distinct immune-brain axis that further amplifies SRI-36 expression and ADF sensitivity, leading to excessive 5-HT release that suppresses food attraction and prioritizes safety. These findings reveal a gut-to-brain mechanism by which metabolic and immune signals converge on central 5-HT to reshape behavioral strategies.