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<p>Ulcerative colitis (UC) is a chronic, relapsing inflammatory disorder characterized by persistent mucosal immune activation and compromised epithelial barrier function. In this study, we identify the RNA-binding protein PUMILIO2 (Pum2) as a previously unrecognized regulator of intestinal inflammation. Analysis of colonic tissues from UC patients revealed reduced Pum2 expression, which inversely correlated with disease activity. In dextran sulfate sodium (DSS)-induced colitis models, Pum2 deficiency exacerbated mucosal injury, accompanied by heightened macrophage inflammation. Mechanistically, Pum2 loss during colitis drives macrophage hyperactivation and TNFα-dependent epithelial necroptosis, which together intensify pathogenic macrophage–epithelial interactions and barrier breakdown. The dynamic downregulation of Pum2 in active inflammation underscores its potential as a therapeutic target for modulating macrophage–epithelial interactions and restoring intestinal barrier integrity in the context of colitis.</p><p></p>

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Loss of Pum2 exacerbates colitis by disrupting macrophage–epithelial crosstalk and promoting epithelial necroptosis

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年3月20日

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  • Xuefei Wang,
  • Xiaoxiao Han,
  • Wenlin Qiu,
  • Lijuan Jiang,
  • Xiaoru Duan,
  • Xiaojing Liu

摘要

Ulcerative colitis (UC) is a chronic, relapsing inflammatory disorder characterized by persistent mucosal immune activation and compromised epithelial barrier function. In this study, we identify the RNA-binding protein PUMILIO2 (Pum2) as a previously unrecognized regulator of intestinal inflammation. Analysis of colonic tissues from UC patients revealed reduced Pum2 expression, which inversely correlated with disease activity. In dextran sulfate sodium (DSS)-induced colitis models, Pum2 deficiency exacerbated mucosal injury, accompanied by heightened macrophage inflammation. Mechanistically, Pum2 loss during colitis drives macrophage hyperactivation and TNFα-dependent epithelial necroptosis, which together intensify pathogenic macrophage–epithelial interactions and barrier breakdown. The dynamic downregulation of Pum2 in active inflammation underscores its potential as a therapeutic target for modulating macrophage–epithelial interactions and restoring intestinal barrier integrity in the context of colitis.