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We have found a previously unknown reaction of human airway epithelial cells to allergens that involves rapid mobilization and release of nuclear DNA from epithelial cells that remain viable throughout the duration of exposure. We found that allergen exposure induces caspase 3 by a non-canonical mechanism that involves calcium-dependent activation of furin and that caspase 3 use contributes to DNA fragmentation, as shown in comet assays. We show that allergen-induced type 2 immune responses are markedly reduced by pretreatment with a DNA scavenger and that nDNA release in mice that were caspase 3 deficient. Moreover, we report that intranasal treatment with mouse genomic DNA, as well as subcutaneous exposure to allergens, improved Th2 cytokines secretion conversion into bronchoalveolar lavage fluid, whereas DNA alone had no effect.
Source link: https://www.ncbi.nlm.nih.gov/bioproject/816531
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