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Bronchoalveolar Lavage Exosomes in Lipopolysaccharide-induced Septic Lung Injury
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Pathologic Th1-Treg Cells Exacerbate Acute Lung Injury and Lethality in Sepsis.

Takuya Murao1, Atsushi Murao1, Monowar Aziz1,2

  • 1Center for Immunology and Inflammation, The Feinstein Institutes for Medical Research, Manhasset, NY 11030, USA.

Cells
|March 27, 2026
PubMed
Summary

Extracellular cold-inducible RNA-binding protein (eCIRP) induces pathogenic Th1-Treg cells via the TLR4-STAT1/5 pathway, worsening sepsis-induced acute lung injury (ALI) and mortality. Targeting these cells may alleviate sepsis complications.

Keywords:
ALISTAT1STAT5TLR4Th1-Treg cellseCIRPsepsis

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Area of Science:

  • Immunology
  • Cell Biology
  • Pathophysiology

Background:

  • Sepsis involves immune dysregulation and acute lung injury (ALI), often leading to high mortality.
  • Extracellular cold-inducible RNA-binding protein (eCIRP) is a damage-associated molecular pattern implicated in sepsis.
  • The role of a specific CD4+ T cell subset, Th1-Treg cells, in sepsis-induced ALI is currently unknown.

Purpose of the Study:

  • To investigate the dynamics, induction mechanisms, and functional roles of Th1-Treg cells in sepsis-induced ALI.
  • To elucidate the involvement of eCIRP, TLR4, and STAT signaling in Th1-Treg cell induction during sepsis.
  • To determine the impact of Th1-Treg cells on ALI severity and mortality in a murine sepsis model.

Main Methods:

  • Polymicrobial sepsis was induced in wild-type (WT) and knockout mice (CIRP-/- and TLR4-/-) via cecal ligation and puncture.
  • Th1-Treg cell accumulation in lungs was assessed in vivo.
  • In vitro, CD4+ T cells were stimulated with eCIRP to analyze Th1-Treg differentiation and STAT1/5 activation.
  • Pharmacological inhibitors and adoptive cell transfer were used to evaluate signaling pathways and functional roles.

Main Results:

  • Sepsis led to significant Th1-Treg cell accumulation in the lungs of WT mice.
  • eCIRP induced Th1-Treg cell differentiation in vitro, an effect dependent on TLR4 and STAT1/5 activation.
  • CIRP-/- mice showed reduced Th1-Treg cell lung accumulation post-sepsis.
  • Adoptive transfer of Th1-Treg cells exacerbated ALI and increased mortality in septic mice.

Conclusions:

  • The eCIRP-TLR4-STAT1/5 axis drives the induction of pathogenic Th1-Treg cells during sepsis.
  • These Th1-Treg cells significantly aggravate sepsis-induced ALI and contribute to increased mortality.
  • Targeting eCIRP-induced Th1-Treg cells presents a potential therapeutic strategy for sepsis-induced ALI.