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<p>Type 1 Diabetes Mellitus (T1DM) is a chronic autoimmune disease characterized by the destruction of pancreatic β-cells. Growing evidence indicates that immune dysregulation along the gut–lung axis contributes to its pathogenesis. This study aimed to develop a selenium-loaded sustained-release Schizophyllan (Se/s-SPG) composite and investigate its mechanism of action in alleviating T1DM-associated inflammatory immune responses through modulation of the gut microbiota and the Toll-like receptor 4 (TLR4)/Nuclear Factor kappa B (NF-κB) signaling pathway. A T1DM model was established using non-obese diabetic (NOD)/LtJ mice. Comprehensive analyses were performed, including 16&#xa0;S rRNA sequencing, RNA sequencing (RNA-seq), Western blot (WB), Enzyme-linked immunosorbent assay (ELISA), and Flow Cytometry to assess the effects of Se/s-SPG on gut microbial diversity, pancreatic structure and function, immune cell subset distribution, and inflammatory signaling pathways. The results demonstrated that Se/s-SPG significantly improved glucose metabolism, restored intestinal and pulmonary barrier integrity, and regulated T cell subset differentiation as well as macrophage polarization. This study proposes a novel intervention strategy targeting the gut–lung axis for T1DM and highlights its potential for clinical translation.</p> Graphical abstract <p></p>

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Selenium-loaded sustained-release schizophyllan alleviates pancreatic and pulmonary inflammatory damage in type 1 diabetes mellitus by modulating gut microbiota and T cell balance

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年3月14日

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  • Junming Luo,
  • Siying Pei,
  • Zhiying Ai,
  • Runqing Rao,
  • Zhuoyuan Yang,
  • Xin Guo,
  • Zeyi Ai,
  • Lilin Fan,
  • Fang Zou

摘要

Type 1 Diabetes Mellitus (T1DM) is a chronic autoimmune disease characterized by the destruction of pancreatic β-cells. Growing evidence indicates that immune dysregulation along the gut–lung axis contributes to its pathogenesis. This study aimed to develop a selenium-loaded sustained-release Schizophyllan (Se/s-SPG) composite and investigate its mechanism of action in alleviating T1DM-associated inflammatory immune responses through modulation of the gut microbiota and the Toll-like receptor 4 (TLR4)/Nuclear Factor kappa B (NF-κB) signaling pathway. A T1DM model was established using non-obese diabetic (NOD)/LtJ mice. Comprehensive analyses were performed, including 16 S rRNA sequencing, RNA sequencing (RNA-seq), Western blot (WB), Enzyme-linked immunosorbent assay (ELISA), and Flow Cytometry to assess the effects of Se/s-SPG on gut microbial diversity, pancreatic structure and function, immune cell subset distribution, and inflammatory signaling pathways. The results demonstrated that Se/s-SPG significantly improved glucose metabolism, restored intestinal and pulmonary barrier integrity, and regulated T cell subset differentiation as well as macrophage polarization. This study proposes a novel intervention strategy targeting the gut–lung axis for T1DM and highlights its potential for clinical translation.

Graphical abstract