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Updated: Jun 15, 2025

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Endothelial CLEC5A drives barrier dysfunction and vascular leakage responsible for lung injury in bacterial pneumonia

Tie-Ning Zhang1, Xin-Mei Huang2, Julie E Goodwin3,4,5

  • 1Department of Pediatrics, Shengjing Hospital of China Medical University, Shenyang 110004, China.

Science Advances
|June 11, 2025
PubMed

Insights

Mice lacking myeloid C-type lectin domain family 5 member A (CLEC5A) showed increased survival in sepsis models. Targeting endothelial CLEC5A may offer a new therapeutic strategy for bacterial infections like pneumonia and sepsis.

Area of Science:

  • Immunology
  • Vascular Biology
  • Microbiology

Background:

  • Endothelial barrier dysfunction contributes to multiorgan failure in sepsis.
  • Myeloid C-type lectin domain family 5 member A (CLEC5A) is a pattern recognition receptor involved in host defense.
  • CLEC5A's role in endothelial barrier integrity during infection is not fully understood.

Purpose of the Study:

  • To investigate the role of CLEC5A in endothelial barrier function during sepsis and bacterial pneumonia.
  • To determine if targeting endothelial CLEC5A could be a therapeutic strategy.

Main Methods:

  • Cecal ligation and puncture (CLP) and lipopolysaccharide (LPS) models of sepsis in mice.
  • Endothelial-specific CLEC5A knockdown and reexpression.
  • Single-cell RNA sequencing of lung vasculature.
  • In vitro assays measuring trans-endothelial electrical resistance and immune cell migration.

Main Results:

  • Mice lacking CLEC5A exhibited reduced mortality in CLP-induced sepsis and LPS-induced endotoxemia.
  • Endothelial-specific CLEC5A deficiency improved survival and alleviated inflammatory storm and vascular leakage.
  • CLEC5A deletion in endothelial cells maintained barrier integrity and reduced immune cell transmigration in vitro.
  • Endothelial CLEC5A deficiency protected against *Escherichia coli*-induced pneumonia.

Conclusions:

  • Endothelial CLEC5A plays a critical role in regulating endothelial barrier function during sepsis and bacterial pneumonia.
  • Targeting endothelial CLEC5A represents a promising therapeutic approach for sepsis and bacterial infections.

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