Interleukin 31 receptor α promotes smooth muscle cell contraction and airway hyperresponsiveness in asthma.
Interleukin 31 receptor α promotes smooth muscle cell contraction and airway hyperresponsiveness in asthma.
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白细胞介素31受体α促进哮喘中的平滑肌细胞收缩和气道高反应性。
DOI：
10.1038/s41467-023-44040-1
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发表时间：
2023-12-11
影响因子：
16.6
通讯作者：
Madala, Satish K.
中科院分区：
文献类型：
--
作者：
Akkenepally, Santhoshi V.;Yombo, Dan J. K.;Yerubandi, Sanjana;Reddy, Geereddy Bhanuprakash;Deshpande, Deepak A.;Mccormack, Francis X.;Madala, Satish K.
Asthma is a chronic inflammatory airway disease characterized by airway hyperresponsiveness (AHR), inflammation, and goblet cell hyperplasia. Multiple cytokines, including IFNγ, IL-4, and IL-13 are associated with asthma; however, the mechanisms underlying the effects of these cytokines remain unclear. Here, we report a significant increase in the expression of IL-31RA, but not its cognate ligand IL-31, in mouse models of allergic asthma. In support of this, IFNγ, IL-4, and IL-13 upregulated IL-31RA but not IL-31 in both human and mice primary airway smooth muscle cells (ASMC) isolated from the airways of murine and human lungs. Importantly, the loss of IL-31RA attenuated AHR but had no effect on inflammation and goblet cell hyperplasia in mice challenged with allergens or treated with IL-13 or IFNγ. We show that IL-31RA functions as a positive regulator of muscarinic acetylcholine receptor 3 expression, augmenting calcium levels and myosin light chain phosphorylation in human and murine ASMC. These findings identify a role for IL-31RA in AHR that is distinct from airway inflammation and goblet cell hyperplasia in asthma. Although IL-31 has been implicated in asthma, the exact contribution of the IL-31 receptor (IL-31RA) signalling to airway hyperresponsiveness remains unexplored. Here, the authors demonstrate that IL31RA promotes muscarinic acetylcholine receptor 3 expression and calcium signalling, as well as smooth muscle cell contraction.
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DOI：
10.1152/ajplung.00013.2006
发表时间：
2006-09-01
影响因子：
4.9
作者：
Gosens, Reinoud;Stelmack, Gerald L.;Halayko, Andrew J.
通讯作者：
Halayko, Andrew J.
影响因子：
14.2
作者：
Cui, JQ;Pazdziorko, S;Marusic, S
通讯作者：
Marusic, S
影响因子：
4.4
作者：
Bilsborough, Janine;Mudri, Sherri;Dillon, Stacey R.
通讯作者：
Dillon, Stacey R.
影响因子：
3.6
作者：
Feld, Micha;Shpacovitch, Victoria M.;Steinhoff, Martin
通讯作者：
Steinhoff, Martin
影响因子：
16.6
作者：
Kuzumi A;Yoshizaki A;Matsuda KM;Kotani H;Norimatsu Y;Fukayama M;Ebata S;Fukasawa T;Yoshizaki-Ogawa A;Asano Y;Morikawa K;Kazoe Y;Mawatari K;Kitamori T;Sato S
通讯作者：
Sato S