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Eosinophil and airway nerve interactions in asthma
Author(s) -
Drake Matthew G.,
Lebold Katherine M.,
RothCarter Quinn R.,
Pincus Alexandra B.,
Blum Emily D.,
Proskocil Becky J.,
Jacoby David B.,
Fryer Allison D.,
Nie Zhenying
Publication year - 2018
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.3mr1117-426r
Subject(s) - bronchoconstriction , sensory nerve , eosinophil , muscarinic acetylcholine receptor , sensory system , parasympathetic nervous system , airway , vagus nerve , reflex , medicine , neuroscience , asthma , immunology , biology , anesthesia , receptor , autonomic nervous system , stimulation , heart rate , blood pressure
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.