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- W4320922224 abstract "Abstract Asthma is a chronic inflammatory airway disease characterized by airway hyperresponsiveness (AHR), inflammation, and goblet cell hyperplasia. Both Th1 and Th2 cytokines, including IFN-γ, IL-4, and IL-13 have been shown to induce asthma; however, the underlying mechanisms remain unclear. We observed a significant increase in the expression of IL-31RA, but not its cognate ligand IL-31 during allergic asthma. In support of this, IFN-γ and Th2 cytokines, IL-4 and IL-13, upregulated IL-31RA but not IL-31 in airway smooth muscle cells (ASMC). Importantly, the loss of IL-31RA attenuated AHR but had no effects on inflammation and goblet cell hyperplasia in allergic asthma or mice treated with IL-13 or IFN-γ. Mechanistically, we demonstrate that IL-31RA functions as a positive regulator of muscarinic acetylcholine receptor 3 expression and calcium signaling in ASMC. Together, these results identified a novel role for IL-31RA in AHR distinct from airway inflammation and goblet cell hyperplasia in asthma." @default.
- W4320922224 created "2023-02-16" @default.
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- W4320922224 creator A5087723386 @default.
- W4320922224 date "2023-02-15" @default.
- W4320922224 modified "2023-10-18" @default.
- W4320922224 title "Interleukin 31 receptor alpha augments muscarinic acetylcholine receptor 3-driven calcium signaling and airway hyperresponsiveness in asthma" @default.
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- W4320922224 doi "https://doi.org/10.21203/rs.3.rs-2564484/v1" @default.
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- W4320922224 hasPublicationYear "2023" @default.
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