Aspergillus niger conidia induces asthma in mice.

Asthma results from immune tolerance failure. Commonly used asthma models avoid tolerance by injection of antigens. Our group developed a more physiologically relevant asthma model using potent allergen inhalation. These allergens contain proteinase activities which produce and sustain an asthma phenotype. Preliminary work using dust indicated the homes of asthmatic children contain mainly fungal proteinases. Aspergillus niger (AN) was a common dust isolate and produced a strong proteinase activity similar to that observed in dust. Daily intra‐nasal challenge with as few as 50,000 live (but not sterilized) AN conidia in C57/Bl6 mice is sufficient to establish an asthma phenotype including airway hyper‐reactivity, eosinophilia, and elevated interleukin‐4 secretion in the lung. The asthma phenotype is weak in mice exposed to 5,000 and 10,000 conidia, but the combination of conidia and ovalbumin (a benign antigen) increased the asthma phenotype. Viable fungus persisted in the lungs of C57/Bl6 for over seven days after a single exposure of 400,000 conidia. Sterilized AN conidia were not able to induce asthma phenotype. This data lends support for the concept that some asthma could result from persistence of fungal exposure and possibly low grade fungal infection. This research may shed new light onto the underlying cause of asthma and result in the development of better clinical care treatments.