Neutrophil heterogeneity and fate in inflamed tissues: implications for the resolution of inflammation

János G. Filep, Amiram Ariel

Research output: Contribution to journalArticlepeer-review

Abstract

Filep JG, Ariel A. Neutrophil heterogeneity and fate in inflamed tissues: implications for the resolution of inflammation. Am J Physiol Cell Physiol 319: C510–C532, 2020. First published July 15, 2020; doi:10.1152/ajpcell.00181.2020.—Neutrophils are polymorphonuclear leukocytes that play a central role in host defense against infection and tissue injury. They are rapidly recruited to the inflamed site and execute a variety of functions to clear invading pathogens and damaged cells. However, many of their defense mechanisms are capable of inflicting collateral tissue damage. Neutrophil-driven inflammation is a unifying mechanism underlying many common diseases. Efficient removal of neutrophils from inflammatory loci is critical for timely resolution of inflammation and return to homeostasis. Accumulating evidence challenges the classical view that neutrophils represent a homogeneous population and that halting neutrophil influx is sufficient to explain their rapid decline within inflamed loci during the resolution of protective inflammation. Hence, understanding the mechanisms that govern neutrophil functions and their removal from the inflammatory locus is critical for minimizing damage to the surrounding tissue and for return to homeostasis. In this review, we briefly address recent advances in characterizing neutrophil phenotypic and functional heterogeneity and the molecular mechanisms that determine the fate of neutrophils within inflammatory loci and the outcome of the inflammatory response. We also discuss how these mechanisms may be harnessed as potential therapeutic targets to facilitate resolution of inflammation.

Original languageEnglish
Pages (from-to)C510-C532
JournalAmerican Journal of Physiology - Cell Physiology
Volume319
Issue number3
DOIs
StatePublished - Sep 2020

Bibliographical note

Publisher Copyright:
© 2020 the American Physiological Society

Keywords

  • Cell death
  • Efferocytosis
  • Neutrophil trafficking
  • Neutrophils
  • Specialized proresolving mediators
  • Neutrophils/cytology
  • Homeostasis/physiology
  • Humans
  • Inflammation/metabolism
  • Host-Derived Cellular Factors/metabolism
  • Phenotype
  • Animals
  • Apoptosis/physiology

ASJC Scopus subject areas

  • Physiology
  • Cell Biology

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