Interleukin 31 receptor α promotes smooth muscle cell contraction and airway hyperresponsiveness in asthma

Santhoshi V. Akkenepally, Dan J. K. Yombo, Sanjana Yerubandi, Geereddy Bhanuprakash Reddy, Deepak A. Deshpande, Francis X. McCormack and Satish K. Madala ()
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Santhoshi V. Akkenepally: University of Cincinnati
Dan J. K. Yombo: Cincinnati Children’s Hospital Medical Center
Sanjana Yerubandi: University of Cincinnati
Geereddy Bhanuprakash Reddy: National Institute of Nutrition
Deepak A. Deshpande: Sidney Kimmel Medical College, Thomas Jefferson University
Francis X. McCormack: University of Cincinnati
Satish K. Madala: University of Cincinnati

Nature Communications, 2023, vol. 14, issue 1, 1-19

Abstract: Abstract 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.

Date: 2023
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DOI: 10.1038/s41467-023-44040-1

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