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Young bakery apprentices incur substantial exposure to known airways allergens, a situation that might elicit early induction of airways inflammation.
The method consists of the induction of airways secretions after the inhalation of progressively increased concentrations of saline aerosol.
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However, repeated exposure to large numbers may result in persistence of conidia and induction of airway inflammation.
Lastly, a comparative analysis of inflammation and sensitization outputs reveals that the development of the latter is more sensitive to allergen than the induction of airway inflammation.
Our model suggests that the induction of airway CD8+ T cell responses to A. fumigatus conidia is mediated in part by the ability to germinate at physiological temperatures.
These data suggest a correlation between the ability of conidia to germinate in vivo and the induction of airway immune responses to Aspergillus aspiration.
Eosinophils activated by IL-3 contribute to T cell activation in allergic diseases [111] and play a critical role in the induction of airway hyperreactivity and the development of lesions that underpin chronic airway wall remodelling [112].
Predominance of Th2 cytokines in murine models of acute allergic airway inflammation is well established [15] and important roles of IL-5 in induction of airway eosinophilia and of IL-5, IL-4 and IL-13 in the development of AHR [16], [17] have been defined.
CNT also generate reactive oxygen species [ 25], which probably plays an additional role in their induction of airway allergic inflammation.
Analysis of the gene ontologies stimulated by PM in naive mice demonstrated similarities to prior PM-related genomic studies with the induction of airway inflammation activity.
Moreover, it has been revealed that reduced NADPH oxidase is present in the pollen grains and can lead to induction of airway associated oxidative stress.
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