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- W1993398535 abstract "Although alteration of airway pH may serve an innate host defense capacity, it also is implicated in the pathophysiology of obstructive airway diseases. Acid-induced asthma appears in association with gastroesophageal reflux after accidental inhalation of acid (fog, pollution, and workplace exposure) and in the presence of altered airway pH homeostasis. Endogenous and exogenous exposures to acids evoke cough, bronchoconstriction, airway hyperreactivity, microvascular leakage, and heightened production of mucous, fluid, and nitric oxide. Abnormal acidity of the airways is reflected in exhaled breath assays. The intimate mechanisms of acid-induced airway obstruction are dependent on activation of capsaicin-sensitive sensory nerves. Protons activate these nerves with the subsequent release of tachykinins (major mediators of this pathway) that, in conjunction with kinins, nitric oxide, oxygen radicals, and proteases, modulate diverse aspects of airway dysfunction and inflammation. The recognition that acid stress might initiate or exacerbate airway obstructive symptomatology has prompted the consideration of new therapies targeting pH homeostasis." @default.
- W1993398535 created "2016-06-24" @default.
- W1993398535 creator A5041462222 @default.
- W1993398535 creator A5050285523 @default.
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- W1993398535 date "2004-04-01" @default.
- W1993398535 modified "2023-10-17" @default.
- W1993398535 title "Acid stress in the pathology of asthma" @default.
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- W1993398535 doi "https://doi.org/10.1016/j.jaci.2003.12.034" @default.
- W1993398535 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/15100663" @default.
- W1993398535 hasPublicationYear "2004" @default.
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