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<p>The psychological state profoundly influences immune responses. While chronic stress is generally known to exacerbate inflammation, the impact of acute stress on inflammation has received far less attention. Here, we report that acute stress suppressed group 2 innate lymphoid cell (ILC2) responses, thereby alleviating type 2 lung inflammation. Restraint stress-induced acute stress activated the hypothalamic–pituitary–adrenal (HPA) axis and subsequently increased corticosterone levels. Corticosterone protected mice against lung inflammation by limiting ILC2 proliferation and type 2 cytokine production via the glucocorticoid receptor (GR). Adrenalectomy and genetic perturbation of the GR in ILC2s abolished acute stress-mediated immunosuppressive effects. Mechanistic studies revealed that corticosterone-GR signaling impaired ILC2 responses to microenvironmental factors by dampening downstream NF-κB and JAK-STAT signaling. Collectively, these findings reveal that acute stress alleviates ILC2-mediated lung inflammation through the neuroendocrine circuit and demonstrate the inhibitory role of endogenous corticosterone in ILC2 responses.</p>

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Acute stress alleviates type 2 lung inflammation by restricting ILC2s through corticosterone-glucocorticoid receptor signaling

  • 期刊论文

  • 发表日期：

    2026年4月2日

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  • Lin Zhu,
  • Yuying Huang,
  • Bo Peng,
  • Shufeng Zhong,
  • Xiaoyu Zhang,
  • Fuyang Xiao,
  • Dilare Asim,
  • Jieken Pakezhati,
  • Jinquan Ma,
  • Siying Sun,
  • Jiefang Xu,
  • Shipeng Cheng,
  • Liyan Ma,
  • Zhiyang Ling,
  • Chuyan Yi,
  • Dongmei Lu,
  • Junqin Liang,
  • Bing Sun

摘要

The psychological state profoundly influences immune responses. While chronic stress is generally known to exacerbate inflammation, the impact of acute stress on inflammation has received far less attention. Here, we report that acute stress suppressed group 2 innate lymphoid cell (ILC2) responses, thereby alleviating type 2 lung inflammation. Restraint stress-induced acute stress activated the hypothalamic–pituitary–adrenal (HPA) axis and subsequently increased corticosterone levels. Corticosterone protected mice against lung inflammation by limiting ILC2 proliferation and type 2 cytokine production via the glucocorticoid receptor (GR). Adrenalectomy and genetic perturbation of the GR in ILC2s abolished acute stress-mediated immunosuppressive effects. Mechanistic studies revealed that corticosterone-GR signaling impaired ILC2 responses to microenvironmental factors by dampening downstream NF-κB and JAK-STAT signaling. Collectively, these findings reveal that acute stress alleviates ILC2-mediated lung inflammation through the neuroendocrine circuit and demonstrate the inhibitory role of endogenous corticosterone in ILC2 responses.