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Related Experiment Video

Updated: Jun 5, 2025

A Controlled Mouse Model for Neonatal Polymicrobial Sepsis
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INDUCTION OF EARLY PULMONARY SENESCENCE IN EXPERIMENTAL SEPSIS.

Martin Mösenlechner1, Daniela Schlösser2, Sonja Braumüller1

  • 1Institute of Clinical and Experimental Trauma-Immunology, University Medical Center Ulm, Ulm, Germany.

Shock (Augusta, Ga.)
|December 5, 2024
PubMed
Summary

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Sepsis activates cellular senescence pathways in the lungs, indicated by increased p21 expression and altered CD47-SHP-1 axis. Further research is needed to understand long-term effects of sepsis-induced senescence.

Area of Science:

  • Immunology
  • Cell Biology
  • Pathophysiology

Background:

  • Sepsis poses a significant global health threat and economic burden.
  • Cellular senescence, including CD47-mediated efferocytosis suppression, is increasingly understood.
  • The impact of cell stress in systemic illnesses like sepsis is poorly understood in vivo.

Purpose of the Study:

  • Investigate molecular alterations in senescence-associated pulmonary mechanisms during experimental sepsis.
  • Analyze changes in lung tissue and associated biochemical markers post-sepsis induction.

Main Methods:

  • Utilized a cecal ligation and puncture (CLP) model in male C57BL/6JRj mice to induce sepsis.
  • Harvested blood, bronchoalveolar fluids, and lungs at 24 hours and 7 days post-CLP for analysis.

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Last Updated: Jun 5, 2025

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  • Assessed histological damage, plasma surfactant protein D, and pulmonary expression of senescence markers (p16, p21) and the CD47-QPCTL-SHP-1 axis.

    • Main Results:

    • CLP induced histological lung damage and elevated plasma surfactant protein D, indicating acute lung injury.
    • Observed significant upregulation of the CD47-QPCTL-SHP-1 axis in septic mouse lungs.
    • Found decreased p16 but increased p21 expression in septic lungs; CD47/QPCTL decreased while SHP-1 increased by day 7.

    Conclusions:

    • Experimental sepsis activates senescence-associated pathways in the lungs.
    • Early senescence marker p21 is upregulated, while late marker p16 is downregulated.
    • Further in vivo studies are required to elucidate long-term consequences of sepsis-induced cellular senescence.