Eosinophil and airway nerve interactions in asthma

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

Research output: Contribution to journalReview articlepeer-review

47 Scopus citations


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 M 2 muscarinic receptors on parasympathetic nerves. Loss of M 2 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
Issue number1
StatePublished - Jul 2018


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

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Cell Biology


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