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Effects of pollen season on central and peripheral nitric oxide production in subjects with pollen asthma

Journal article
Authors Björn Bake
Emilia Viklund
Anna-Carin Olin
Published in Respiratory Medicine
Volume 108
Issue 9
Pages 1277-1283
ISSN 0954-6111
Publication year 2014
Published at Institute of Medicine, Department of Public Health and Community Medicine, Section of Occupational and environmental medicine
Institute of Medicine
Pages 1277-1283
Language en
Links dx.doi.org/10.1016/j.rmed.2014.06.0...
Keywords Pollen, Asthma, NO, Alveolar, Peripheral, FENO, AXIAL DIFFUSION, BRONCHIAL HYPERRESPONSIVENESS, ALLERGIC RHINITIS, EXCHANGE DYNAMICS, LUNG-FUNCTION, BREATH-HOLD, EXPOSURE, AIRWAYS, IMPACT, STANDARDIZATION, Cardiac & Cardiovascular Systems, Respiratory System
Subject categories Clinical Medicine

Abstract

Background: Pollen exposure of allergic subjects with asthma causes increased nitric oxide (NO) in exhaled air (FENO) suggestive of increased airway inflammation. It is, however, unclear to what extent NO production in peripheral airways and alveoli are involved. Objectives: The aim of the present investigation was to analyze the relationship between central and peripheral components of FENO to clarify the distribution of pollen induced inflammation in asthma. Subjects and methods: 13 pollen allergic non-smoking subjects with mild-intermittent asthma and 12 healthy non-smoking control subjects were examined with spirometry and FENO at flows between 50 and 270 mL/s during and out of pollen season. Results: Spirometry was normal and unaffected by season in subjects with asthma as well as controls. Out of season subjects with asthma had significantly higher FENO, elevated airway production (JawNO) and preacinar/acinar production (CANO) than controls. Pollen exposure resulted in significantly increased FENO and JawNO but not CANO. FENO among controls were not affected by season. Individual results showed, however, that CANO increased substantially in a few subjects with asthma. The increased CANO in subjects with asthma may be explained by increased NO production in preacinar/acinar airways and back diffusion towards the alveoli. Conclusions: The findings may indicate that subjects with allergic asthma have airway inflammation without alveolar involvement outside the pollen season and pollen exposure causes a further increase of airway inflammation and in a few subjects obstruction of intra acinar airways causing impeded back diffusion. Increased NO production in central airways, unassociated with airway obstruction could be an alternative explanation. These effects were not disclosed by spirometry.

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