Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P15088 (mast cell)
 14,925 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mast cells and eosinophils may play a role in the pathophysiology of chronic cough in nonasthmatics. It is unknown, however, whether degranulation of these cells occurs in the airways of such patients. Thirty-five nonsmoking patients referred with a chronic nonproductive cough (mean cough duration 76.2 months) were evaluated using a comprehensive diagnostic protocol. Bronchoalveolar lavage (BAL) cell differentials and BAL histamine, tryptase and eosinophilic cationic protein (ECP) concentrations were determined. Ten nonsmoking healthy volunteers served as controls. Diagnostic subgroups were identified: eight postnasal drip syndrome (PNDS), seven cough variant asthma (CVA), seven gastro-esophageal reflux (GOR), seven dual aetiology and six idiopathic. Nonasthmatic coughers (NAC) were characterized as those patients without bronchial hyperresponsiveness on histamine challenge and whose cough had either responded to therapy for PNDS or GOR or failed to improve with antiasthma therapy. There was a significant increase in both eosinophil and mast cell numbers (p<0.05) and in histamine levels (p = 0.027) when NAC patients were compared with controls. Tryptase and ECP levels were elevated in 7 of 23 and 6 of 23 NAC patients, respectively. In conclusion, airway inflammatory cell numbers are not only increased but also activated, suggesting an important role for airways inflammation in the pathophysiology of chronic nonproductive cough.
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PMID:Bronchoalveolar lavage findings in patients with chronic nonproductive cough. 1083 24

Cough variant asthma and the closely related corticosteroid responsive cough syndromes eosinophilic bronchitis and atopic cough are common causes of chronic cough. The diagnosis is often not overt but detailed investigation of airway responsiveness and airway inflammation can be helpful. Cough variant asthma, eosinophilic bronchitis and atopic cough are all associated with eosinophilic airway inflammation, which is similar to that seen in non-cough predominant asthma. However, evidence of activated mast cells and increased concentrations of mast cell products appears to be confined to the conditions associated with cough, suggesting a role for mast cell degranulation in the superficial airway structures in the pathogenesis of cough. Cough variant asthma is typically corticosteroid responsive; leukotriene antagonists and antihistamines also help. Further study of this interesting asthma variant may increase our understanding of the relationship between airway inflammation and airway dysfunction.
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PMID:Cough and asthma. 1556 83

Most studies agree that post-nasal drip syndrome (PNDS), asthma, gastroesophageal reflux disease (GORD), and laryngopharyngeal reflux (LPR) are the commonest causes of chronic cough in the immunocompetent, non-smoking patient who is not taking an angiotensin-converting enzyme inhibitor. No diagnostic test has been found to define those who are said to have PNDS other than a response to a first-generation antihistamine. Examining the available evidence suggests that mechanical stimulation of the pharynx by mucus is not an adequate theory for the production of cough. Inflammatory mediators in the lower airways are raised in PNDS, cough variant asthma and GORD, and the theory that an inflammatory process is affecting 'one airway' is a plausible one. Nasal disease is more likely to result in cough from the co-existing involvement of the lower airways through an as yet undefined pathway, and eosinophil and mast cell mediation appear a likely mechanism.
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PMID:The aetiology of chronic cough: a review of current theories for the otorhinolaryngologist. 1648 May 51

Among the most common causes of chronic cough are asthma (25%) and nonasthmatic eosinophilic bronchitis (10%). In asthma, cough may present as an isolated symptom, in which case it is known as cough variant asthma. Variable airflow obstruction and airway hyper-responsiveness are cardinal features of asthma, which are absent in nonasthmatic eosinophilic bronchitis. The presence of eosinophilic airway inflammation is a common feature of asthma and is a diagnostic criterion for nonasthmatic eosinophilic bronchitis. At a cellular level, mast cell infiltration into the airway smooth muscle bundle, narrowing of the airway wall, and increased interleukin-13 expression are features of asthma and not nonasthmatic eosinophilic bronchitis. In most cases, the trigger that causes the cough is uncertain, but occasionally occupational exposure to a sensitizer is identified, and avoidance is recommended. In both conditions, there is improvement following treatment with inhaled corticosteroids, which is associated with the presence of an airway eosinophilia and increased exhaled nitric oxide. Generally, response to therapy in both conditions is very good, and the limited long-term data available suggest that both usually have a benign course, although in some cases fixed airflow obstruction may occur.
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PMID:Cough due to asthma, cough-variant asthma and non-asthmatic eosinophilic bronchitis. 2017 62