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<p>The development of novel therapeutic strategies for allergic rhinitis (AR) remains a pressing need, and the potential role and mechanisms of basic fibroblast growth factor (bFGF) in AR treatment are still unclear. This study aimed to investigate whether bFGF alleviates AR by restoring nasal epithelial barrier function through the modulation of autophagy. An ovalbumin (OVA)-induced AR model was established in BALB/c mice, which then received intranasal bFGF (10&#xa0;μg/day) either alone or in combination with intraperitoneal injection of the autophagy activator rapamycin (RAPA, 0.5&#xa0;mg/kg/day). bFGF treatment significantly alleviated AR symptoms (<i>p</i> &lt; 0.01), reduced levels of OVA-specific IgE and Th2 cytokines (IL-4, IL-5, IL-13) in serum and bronchoalveolar lavage fluid, and suppressed inflammatory cell infiltration and goblet cell hyperplasia in nasal tissue. Moreover, bFGF upregulation of tight junction proteins (ZO-1, occludin, and claudin-1) was accompanied by inhibition of autophagy, indicated by reduced LC3-II and Beclin-1 levels and elevated p62 expression. Importantly, all therapeutic effects of bFGF were reversed by RAPA co-administration (<i>p</i> &lt; 0.05). These findings demonstrate that bFGF suggesting that bFGF may enhance nasal barrier integrity in association with suppression of pathological autophagy, suggesting a promising novel treatment strategy for AR.</p>

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bFGF inhibits autophagy and restores mucosal barrier integrity in allergic rhinitis mice

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月24日

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  • Xiaoqiong Wang,
  • Menglu Xu,
  • Hanchi Chen,
  • Xuejun Liu,
  • Liyan Ni

摘要

The development of novel therapeutic strategies for allergic rhinitis (AR) remains a pressing need, and the potential role and mechanisms of basic fibroblast growth factor (bFGF) in AR treatment are still unclear. This study aimed to investigate whether bFGF alleviates AR by restoring nasal epithelial barrier function through the modulation of autophagy. An ovalbumin (OVA)-induced AR model was established in BALB/c mice, which then received intranasal bFGF (10 μg/day) either alone or in combination with intraperitoneal injection of the autophagy activator rapamycin (RAPA, 0.5 mg/kg/day). bFGF treatment significantly alleviated AR symptoms (p < 0.01), reduced levels of OVA-specific IgE and Th2 cytokines (IL-4, IL-5, IL-13) in serum and bronchoalveolar lavage fluid, and suppressed inflammatory cell infiltration and goblet cell hyperplasia in nasal tissue. Moreover, bFGF upregulation of tight junction proteins (ZO-1, occludin, and claudin-1) was accompanied by inhibition of autophagy, indicated by reduced LC3-II and Beclin-1 levels and elevated p62 expression. Importantly, all therapeutic effects of bFGF were reversed by RAPA co-administration (p < 0.05). These findings demonstrate that bFGF suggesting that bFGF may enhance nasal barrier integrity in association with suppression of pathological autophagy, suggesting a promising novel treatment strategy for AR.