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Acid-Sensing Ion Channel 1a Contributes to Airway Hyperreactivity in Mice
Journal article   Open access   Peer reviewed

Acid-Sensing Ion Channel 1a Contributes to Airway Hyperreactivity in Mice

Leah R Reznikov, David K Meyerholz, Ryan J Adam, Mahmoud Abou Alaiwa, Omar Jaffer, Andrew S Michalski, Linda S Powers, Margaret P Price, David A Stoltz and Michael J Welsh
PloS one, Vol.11(11), pp.e0166089-e0166089
2016
DOI: 10.1371/journal.pone.0166089
PMCID: PMC5098826
PMID: 27820848
url
https://doi.org/10.1371/journal.pone.0166089View
Published (Version of record) Open Access

Abstract

Neurons innervating the airways contribute to airway hyperreactivity (AHR), a hallmark feature of asthma. Several observations suggested that acid-sensing ion channels (ASICs), neuronal cation channels activated by protons, might contribute to AHR. For example, ASICs are found in vagal sensory neurons that innervate airways, and asthmatic airways can become acidic. Moreover, airway acidification activates ASIC currents and depolarizes neurons innervating airways. We found ASIC1a protein in vagal ganglia neurons, but not airway epithelium or smooth muscle. We induced AHR by sensitizing mice to ovalbumin and found that ASIC1a-/- mice failed to exhibit AHR despite a robust inflammatory response. Loss of ASIC1a also decreased bronchoalveolar lavage fluid levels of substance P, a sensory neuropeptide secreted from vagal sensory neurons that contributes to AHR. These findings suggest that ASIC1a is an important mediator of AHR and raise the possibility that inhibiting ASIC channels might be beneficial in asthma.
Asthma - metabolism Vagus Nerve - metabolism Mice, Inbred C57BL Respiratory Hypersensitivity - metabolism Male Nerve Tissue Proteins - metabolism Inflammation - metabolism Animals Respiratory System - metabolism Substance P - metabolism Mice Sensory Receptor Cells - metabolism Bronchoalveolar Lavage Fluid - chemistry Acid Sensing Ion Channels - metabolism

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