Opening the flood-gates: how neutrophil-endothelial interactions regulate permeability

Matthew R. DiStasi, Klaus Ley

Research output: Contribution to journalReview articlepeer-review

176 Scopus citations


Many diseases have an inflammatory component, where neutrophil interactions with the vascular endothelium lead to barrier dysfunction and increased permeability. Neutrophils increase permeability through secreted products such as the chemokines CXCL1, 2, 3, and 8, through adhesion-dependent processes involving β2 integrins interacting with endothelial ICAM-1, and through combinations where β2 integrin engagement leads to degranulation and secretion of heparin-binding protein. Some neutrophil products, such as arachidonic acid or the leukotriene LTA4, are further processed by endothelial enzymes via transcellular metabolism before the resulting products thromboxane A2 or LTC4 can activate their cognate receptors. Neutrophils also generate reactive oxygen species that induce vascular leakage. This review focuses on the mechanisms of neutrophil-mediated leakage.

Original languageEnglish (US)
Pages (from-to)547-556
Number of pages10
JournalTrends in Immunology
Issue number11
StatePublished - Nov 2009
Externally publishedYes

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology


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