Presenting Author: Diandra Ellis
, Doctoral Candidate at Tulane Univ. Sch. of Med.
Abstract:
Chitin, a polysaccharide found in the fungal cell wall and exoskeletons of house dust mites and cockroaches, has garnered attention as a potential immunoreactive allergen. Mammals have evolved to express chitin-degrading chitinases that may modulate immune responses to chitin. We have previously reported that mice deficient in acidic mammalian chitinase (AMCase, Chia) demonstrated better lung function (i.e. airway hyperresponsiveness, AHR) during allergic fungal asthma. Here, we show that during allergic fungal asthma, mice overexpressing AMCase (SPAM mice) had worse lung function, and chitin-bearing conidia from Aspergillus fumigatus are detectable in the lung. The lung function of mutant mice directly correlated with the level of chitinase activity during allergic fungal asthma (Chia-/- mice, low chitinase activity, lower AHR; SPAM mice, high chitinase activity, higher AHR), suggesting that chitin catabolism promoted AHR. Chronic exposure of normal mice to purified chitin from A. fumigatus resulted in moderate inflammatory changes in the lung, however this was not sufficient to induce AHR. Moreover, chronic exposure of mutant mice to purified chitin did not induce AHR. Collectively, these results indicate that 1) fungal chitin alone is incapable of driving AHR and 2) chitinase-mediated degradation of A. fumigatus chitin may facilitate unmasking and/or liberation of other fungal cell wall components that preferentially drive inflammatory responses which contribute to AHR.
Fungal Chitin Does Not Contribute To Allergic Asthma Severity
Category
Poster and Podium (Block Symposium)
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Date: May 5 Presentation Time: 11:30 AM to 12:45 PM Room: Exhibit Hall F1