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A Microphysiological System to Study Leukocyte-Endothelial Cell Interaction during Inflammation
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Extracellular CIRP (eCIRP) and inflammation.

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Extracellular cold-inducible RNA-binding protein (eCIRP) promotes inflammation and organ damage during sepsis and shock. Targeting eCIRP offers a promising therapeutic strategy for inflammatory diseases.

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Area of Science:

  • Immunology
  • Molecular Biology
  • Pathobiology

Background:

  • Cold-inducible RNA-binding protein (CIRP) was initially identified as a cold stress adaptation factor.
  • Intracellular CIRP (iCIRP) is a known stress-response protein.
  • Extracellular CIRP (eCIRP) functions as a damage-associated molecular pattern, crucial in inflammatory diseases.

Purpose of the Study:

  • To review the pathobiology of extracellular CIRP (eCIRP).
  • To emphasize signal transduction pathways involved in eCIRP's inflammatory actions.
  • To explore novel therapeutic interventions targeting eCIRP.

Main Methods:

  • Review of existing literature on CIRP, inflammation, and related signaling pathways.
  • Analysis of studies involving CIRP knockout mice (CIRP-/-).
  • Investigation of eCIRP's interaction with TLR4-MD2 receptors.

Main Results:

  • eCIRP translocates to the extracellular space during hemorrhagic shock and sepsis.
  • eCIRP induces inflammatory responses in immune cells and endothelial cells.
  • eCIRP activates NF-κB, inflammasome, and mitochondrial DNA damage pathways, leading to cell death.
  • CIRP-/- mice show protection against inflammation.

Conclusions:

  • eCIRP is a key mediator of inflammation and tissue damage in critical illnesses.
  • eCIRP represents a novel drug target for treating inflammatory conditions.
  • Therapeutic strategies involving anti-CIRP antibodies or peptides show potential for sepsis and acute lung injury.