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There were no changes in airway responsiveness or inflammatory response in sheep that received Nogatoxin by tracheal instillation, suggesting that the compound is not a respiratory sensitizer.
Using a model of natural allergen exposure, we examined the effect of regular treatment with salmeterol on allergen-induced changes in airway responsiveness and exhaled nitric oxide (ENO).
To determine the effect of cessation of exposure to pollen on airway responsiveness to adenosine 5′-monophosphate (AMP) in subjects with pollen-induced rhinitis, and to explore the relationship between changes in airway responsiveness and changes in exhaled nitric oxide (ENO) levels.
Previous findings support the concept that IL-9 may play a significant role in mediating both pro-inflammatory and changes in airway responsiveness that characterizes the atopic asthmatic state.
Collectively, these findings support the concept that IL-9 may significantly be involved in mediating both pro-inflammatory and changes in airway responsiveness that characterizes the atopic asthmatic state.
After each MCh challenge, the respiratory system resistance was recorded by animal pulmonary function analysis software, testing baseline airway resistance and Re, which represents changes in airway responsiveness.
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There was also no significant change in airway responsiveness measured by cold air or methacholine challenge (data not shown).
Thus, the effects of SS-induced NGF release on airway SP innervation during prenatal and early postnatal life, when the airways are undergoing intense growth and development, might cause a change in airway responsiveness when exposed to SS much later in life.
The study measured only changes in airways responsiveness to AMP challenge, which is a useful marker of corticosteroid anti-inflammatory activity but also of the effects of the LABA component [ 16, 17].
We observed no significant modification in airway responsiveness to methacholine after formaldehyde exposure at this time (8 hr after exposure).
Consistent with this murine model of asthma, we observed significant increases in airway responsiveness in OVA-treated mice, with PM exposure inducing significant changes in AHR in both naive mice and OVA-induced asthmatic mice.
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