Endothelial cell, but not neutrophil, programmed cell death receptor-ligand 1 loss has a morbid impact on experimental murine shock/sepsis-induced lung injury - Summary - MDSpire

Endothelial cell, but not neutrophil, programmed cell death receptor-ligand 1 loss has a morbid impact on experimental murine shock/sepsis-induced lung injury

  • By

  • Elizabeth W. Tindal

  • Chun-Shiang Chung

  • Yaping Chen

  • Runping Zhao

  • Fernando Gutierrez Garcia

  • Theopi Rados

  • Sean F. Monaghan

  • Alfred Ayala

  • June 2, 2026

  • 0 min

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Objective:

To test the hypothesis that endothelial cell deficiency of PD-L1 differentially contributes to shock/sepsis-induced lung injury/death compared to neutrophil deficiency.

Key Findings:
  • ecPD-L1−/− mice showed lower 14-day mortality compared to Controls after Hem/CLP.
  • Mortality increased in pmnPD-L1−/− mice compared to Controls.
  • Lung vascular permeability decreased in ecPD-L1−/− Hem/CLP mice, but not in pmnPD-L1−/− mice.
  • Cytokine and chemokine levels were altered in ecPD-L1−/− mice, with declines in MCP-1 and blood urea nitrogen.
  • Increased levels of Angiopoietin 2 and BALF MIP-2 and IL-6 were observed in pmnPD-L1−/− animals.
Interpretation:

The results suggest that PD-L1 expression on endothelial cells has a detrimental effect on lung injury, while PD-L1 on neutrophils may play a protective role.

Limitations:
Conclusion:

The study supports the hypothesis that PD-L1 on endothelial cells contributes negatively to lung injury in shock/sepsis, while PD-L1 on neutrophils may have a protective role.

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