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Elevated intrathymic sphingosine-1-phosphate promotes thymus involution during sepsis.

Laura Kuchler1, Lisa K Sha1, Annika K Giegerich1

  • 1Institute of Biochemistry I - Pathobiochemistry, Faculty of Medicine, Goethe-University Frankfurt, 60590 Frankfurt, Germany.

Molecular Immunology
|August 29, 2017
PubMed
Summary

Inhibition of sphingosine kinase (SK) during sepsis prevents thymus atrophy and T cell loss. This strategy restores T cell egress, potentially improving outcomes in sepsis by reducing apoptosis and IL-6 levels.

Keywords:
ApoptosisSepsisSphingosine-1-phosphateT cellsThymus involution

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Area of Science:

  • Immunology
  • Molecular Biology
  • Pharmacology

Background:

  • Sepsis causes thymus atrophy, characterized by thymocyte loss and peripheral lymphopenia, impairing immune response.
  • Interleukin-6 (IL-6) and sphingosine-1-phosphate (S1P) signaling are key mediators of sepsis-induced thymus involution.
  • A disrupted S1P gradient between lymphoid organs and circulation impairs T cell egress during sepsis.

Purpose of the Study:

  • To investigate if inhibiting S1P generation can ameliorate thymus involution during sepsis.
  • To explore the role of sphingosine kinases (SK) in sepsis-induced thymus atrophy.

Main Methods:

  • Sepsis was induced in mice using cecal ligation and puncture (CLP).
  • Mice were treated with a sphingosine kinase inhibitor (SK I-II) post-CLP.
  • Thymus weight, thymocyte apoptosis, peripheral T cell counts, IL-6 expression, and S1P levels were analyzed.

Main Results:

  • SK I-II treatment prevented thymus atrophy, preserving thymus weight and reducing thymocyte apoptosis.
  • Treatment led to lymphocytosis (increased T cells) and decreased IL-6 expression.
  • SK I-II administration maintained the S1P gradient and prevented sphingosine-1-phosphate receptor 1 internalization.

Conclusions:

  • Inhibition of sphingosine kinase and subsequent S1P generation during sepsis restores thymic T cell egress.
  • This approach may offer a therapeutic strategy to improve immune function and outcomes in sepsis.