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We've discovered a previously unknown reaction of human airway epithelial cells to allergens that involves rapid mobilization and leakage of nuclear DNA from epithelial cells that remain viable throughout the duration of exposure. Capase 3 is caused by a non-canonical process that involves calcium-dependent activation of furin, and caspase 3 involvement leads to DNA fragmentation, as shown in comet assays. Pretreatment with a DNA scavenger and that nDNA release was significantly reduced in mice that were caspase 3 deficient mice using a mouse model of allergic inflammation. In addition, we report that intranasal therapy with mouse genomic DNA, as well as subcutaneous exposure to allergens, increased the secretion of Th2 cytokines into bronchoalveolar lavage fluid, while DNA alone had no effect. DNA samples from three biological replicates were collected for DNA sequencing. Extracellular DNA samples from three biological replicates were collected for DNA sequencing.
Source link: https://www.ncbi.nlm.nih.gov/bioproject/816531
FK506 inhibited airway inflammation triggered by Papain, a protease allergen, and RNAseq analysis of lung innate cells, as well as the induction of TH2 cells, which cause chronic inflammation, in a mouse model of airway inflammation caused by chronic inflammation. Our results support the clinical value of FK506 for the treatment of allergen-induced airway inflammation, and help identify the intended and mechanism of action.
Source link: https://www.ncbi.nlm.nih.gov/bioproject/785555
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