Eosinophil and airway nerve interactions in asthma

Matthew Drake, Katherine M. Lebold, Quinn R. Roth-Carter, Alexandra B. Pincus, Emily D. Blum, Becky J. Proskocil, David Jacoby, Allison Fryer, Zhenying (Jane) Nie

Research output: Contribution to journalReview article

15 Scopus citations

Abstract

Airway eosinophils are increased in asthma and are especially abundant around airway nerves. Nerves control bronchoconstiction and in asthma, airway hyperreactivity (where airways contract excessively to inhaled stimuli) develops when eosinophils alter both parasympathetic and sensory nerve function. Eosinophils release major basic protein, which is an antagonist of inhibitory M2 muscarinic receptors on parasympathetic nerves. Loss of M2 receptor inhibition potentiates parasympathetic nerve-mediated bronchoconstriction. Eosinophils also increase sensory nerve responsiveness by lowering neurons’ activation threshold, stimulating nerve growth, and altering neuropeptide expression. Since sensory nerves activate parasympathetic nerves via a central neuronal reflex, eosinophils’ effects on both sensory and parasympathetic nerves potentiate bronchoconstriction. This review explores recent insights into mechanisms and effects of eosinophil and airway nerve interactions in asthma.

Original languageEnglish (US)
Pages (from-to)61-67
Number of pages7
JournalJournal of Leukocyte Biology
Volume104
Issue number1
DOIs
StatePublished - Jul 1 2018

Keywords

  • asthma
  • eosinophil
  • major basic protein
  • parasympathetic nerve
  • sensory nerve

ASJC Scopus subject areas

  • Immunology
  • Cell Biology

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