In asthmatic subjects, the degree of bronchial hyperresponsiveness correlates with the severity of asthma and the amount of treatment required to control asthma. Both in normal and in asthmatic subjects, the degree of airway responsiveness may increase after viral infections, exposure to oxidant pollutants and allergens or sensitizing agents; however, airway hyperresponsiveness is quite stable in the absence of exposure to inflammatory stimuli, suggesting that there are at least two components in airway hyperresponsiveness: a transient component, caused by airway inflammation, and a long-lasting one, unrelated to exposure to acute inflammatory stimuli, which is hypothesized to be due to changes in the autonomic innervation or in the smooth muscle itself.
Pathogenesis of bronchial hyperresponsiveness / Fabbri, Leonardo; P., Boschetto; E., Zocca; N., De Marzo; S., Crescioli; P., Maestrelli; C. E., Mapp. - In: RESPIRATION. - ISSN 0025-7931. - STAMPA. - 54 Suppl 1:(1988), pp. 90-94.
Pathogenesis of bronchial hyperresponsiveness.
FABBRI, Leonardo;
1988
Abstract
In asthmatic subjects, the degree of bronchial hyperresponsiveness correlates with the severity of asthma and the amount of treatment required to control asthma. Both in normal and in asthmatic subjects, the degree of airway responsiveness may increase after viral infections, exposure to oxidant pollutants and allergens or sensitizing agents; however, airway hyperresponsiveness is quite stable in the absence of exposure to inflammatory stimuli, suggesting that there are at least two components in airway hyperresponsiveness: a transient component, caused by airway inflammation, and a long-lasting one, unrelated to exposure to acute inflammatory stimuli, which is hypothesized to be due to changes in the autonomic innervation or in the smooth muscle itself.
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