Journal
JOURNAL OF LEUKOCYTE BIOLOGY
Volume 104, Issue 1, Pages 61-67Publisher
WILEY
DOI: 10.1002/JLB.3MR1117-426R
Keywords
asthma; eosinophil; major basic protein; parasympathetic nerve; sensory nerve
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Funding
- NHLBI NIH HHS [T32 HL083808, R01 HL131525, L30 HL124541, F30 HL132414, K08 HL121254] Funding Source: Medline
- NIEHS NIH HHS [R01 ES017592] Funding Source: Medline
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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. Eosinophils are recruited to airway nerves and cause excessive bronchoconstriction in asthma by altering nerve function.
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