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Bronchial Responsiveness Is Related to Increased Exhaled NO (FE(NO)) in Non-Smokers and Decreased FE(NO) in Smokers
RATIONALE: Both atopy and smoking are known to be associated with increased bronchial responsiveness. Fraction of nitric oxide (NO) in the exhaled air (FE(NO)), a marker of airways inflammation, is decreased by smoking and increased by atopy. NO has also a physiological bronchodilating and bronchopr...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Public Library of Science
2012
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3338521/ https://www.ncbi.nlm.nih.gov/pubmed/22563393 http://dx.doi.org/10.1371/journal.pone.0035725 |
Sumario: | RATIONALE: Both atopy and smoking are known to be associated with increased bronchial responsiveness. Fraction of nitric oxide (NO) in the exhaled air (FE(NO)), a marker of airways inflammation, is decreased by smoking and increased by atopy. NO has also a physiological bronchodilating and bronchoprotective role. OBJECTIVES: To investigate how the relation between FE(NO) and bronchial responsiveness is modulated by atopy and smoking habits. METHODS: Exhaled NO measurements and methacholine challenge were performed in 468 subjects from the random sample of three European Community Respiratory Health Survey II centers: Turin (Italy), Gothenburg and Uppsala (both Sweden). Atopy status was defined by using specific IgE measurements while smoking status was questionnaire-assessed. MAIN RESULTS: Increased bronchial responsiveness was associated with increased FE(NO) levels in non-smokers (p = 0.02) and decreased FE(NO) levels in current smokers (p = 0.03). The negative association between bronchial responsiveness and FE(NO) was seen only in the group smoking less <10 cigarettes/day (p = 0.008). Increased bronchial responsiveness was associated with increased FE(NO) in atopic subjects (p = 0.04) while no significant association was found in non-atopic participants. The reported interaction between FE(NO) and smoking and atopy, respectively were maintained after adjusting for possible confounders (p-values<0.05). CONCLUSIONS: The present study highlights the interactions of the relationship between FE(NO) and bronchial responsiveness with smoking and atopy, suggesting different mechanisms behind atopy- and smoking-related increases of bronchial responsiveness. |
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