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Neutrophil trogocytosis during their trans-endothelial migration: role of extracellular CIRP

Satoshi Takizawa1, Yongchan Lee1, Asha Jacob1,2

  • 1Center for Immunology and Inflammation, The Feinstein Institutes for Medical Research, 350 Community Drive, Manhasset, NY, 11030, USA.

Molecular Medicine (Cambridge, Mass.)
|August 8, 2022
PubMed
Abstract

Insights

Extracellular cold-inducible RNA binding protein (eCIRP) enhances neutrophil trogocytosis during trans-endothelial migration. These eCIRP-activated neutrophils exhibit increased pro-inflammatory activity, contributing to acute lung injury.

Area of Science:

  • Immunology
  • Cell Biology

Background:

  • Neutrophils are key innate immune cells, crucial for fighting infections but can cause tissue damage when over-activated.
  • Neutrophil trogocytosis, a form of membrane transfer, influences immune responses.
  • Extracellular cold-inducible RNA binding protein (eCIRP), a damage-associated molecular pattern (DAMP), promotes neutrophil pro-inflammatory activity.

Purpose of the Study:

  • To investigate the role of eCIRP in neutrophil trogocytosis during trans-endothelial migration.
  • To determine the inflammatory potential of neutrophils that have undergone trogocytosis induced by eCIRP.

Main Methods:

  • In vitro trans-endothelial migration (TEM) assay using mouse neutrophils and lung vascular endothelial cells.
  • Assessment of neutrophil trogocytosis in vitro and in bronchoalveolar lavage fluid from an in vivo mouse model of acute lung injury.

Main Results:

  • Neutrophil trogocytosis occurred during TEM, and eCIRP significantly increased its incidence.
  • Trogocytosed neutrophils acquired endothelial membrane components, including JAM-C and VE-cadherin.
  • eCIRP-induced JAM-C positive trogocytosed neutrophils displayed a more pro-inflammatory phenotype and were found in acute lung injury models.

Conclusions:

  • eCIRP induces neutrophil trogocytosis during inflammatory-driven trans-endothelial migration.
  • Trogocytosed neutrophils, particularly JAM-C positive ones, exhibit an exaggerated pro-inflammatory phenotype.
  • This process contributes to the pathogenesis of acute lung injury.
Keywords:
Acute lung injuryInflammationNeutrophilsTrans-migrationTrogocytosiseCIRP

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