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Aim of the study <p>Acute lung injury (ALI) is a common critical condition in the emergency department and is associated with a high mortality rate. Recombinant human urinary trypsin inhibitor (rhUTI), a serine protease inhibitor compounded by genetic engineering technology, is expected to replace UTI, which has been reported to protect multiple organs against inflammation- and/or injury-induced dysfunction. The aim of the present study was to investigate the immunomodulatory effects of rhUTI on splenic dendritic cells (DCs) in LPS-induced ALI mice.</p> Materials and methods <p>RhUTI was administered to mice, and splenic CD11c + DCs were isolated and assessed using flow cytometry for apoptotic or phenotypic analysis. Protein markers and cytokines were determined by western blotting or enzyme-linked immunosorbent assay.</p> Results <p>After treatment with rhUTI, lung injury in LPS-induced ALI mice improved and the survival rate of the mice increased. Treatment with rhUTI could markedly upregulate the levels of co-stimulatory molecules (CD80 and CD86) and major histocompatibility complex class II molecules (MHC-II) on the surface of splenic DC and decreased the apoptosis rate of splenic DCs in LPS-induced ALI mice. In addition, protein levels of markers of endoplasmic reticulum stress (ERS) and ERS-related apoptotic pathways (including GRP78, XBP-1, PERK, caspase-12, and CHOP) were downregulated in the rhUTI-treated group when compared with the LPS-induced ALI group.</p> Conclusions <p>These results suggest that rhUTI protects LPS-induced ALI mice by improving the immune response of splenic DCs and inhibiting excessive ERS-mediated apoptosis.</p>

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Recombinant human urinary trypsin inhibitor improves the immunological function of splenic dendritic cells in mice with acute lung injury

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年7月9日

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  • Tong Wang,
  • Wenna Liu,
  • Jun Li,
  • Yongli Wan,
  • Hang Su,
  • Anlong Qi

摘要

Aim of the study

Acute lung injury (ALI) is a common critical condition in the emergency department and is associated with a high mortality rate. Recombinant human urinary trypsin inhibitor (rhUTI), a serine protease inhibitor compounded by genetic engineering technology, is expected to replace UTI, which has been reported to protect multiple organs against inflammation- and/or injury-induced dysfunction. The aim of the present study was to investigate the immunomodulatory effects of rhUTI on splenic dendritic cells (DCs) in LPS-induced ALI mice.

Materials and methods

RhUTI was administered to mice, and splenic CD11c + DCs were isolated and assessed using flow cytometry for apoptotic or phenotypic analysis. Protein markers and cytokines were determined by western blotting or enzyme-linked immunosorbent assay.

Results

After treatment with rhUTI, lung injury in LPS-induced ALI mice improved and the survival rate of the mice increased. Treatment with rhUTI could markedly upregulate the levels of co-stimulatory molecules (CD80 and CD86) and major histocompatibility complex class II molecules (MHC-II) on the surface of splenic DC and decreased the apoptosis rate of splenic DCs in LPS-induced ALI mice. In addition, protein levels of markers of endoplasmic reticulum stress (ERS) and ERS-related apoptotic pathways (including GRP78, XBP-1, PERK, caspase-12, and CHOP) were downregulated in the rhUTI-treated group when compared with the LPS-induced ALI group.

Conclusions

These results suggest that rhUTI protects LPS-induced ALI mice by improving the immune response of splenic DCs and inhibiting excessive ERS-mediated apoptosis.