Nicotinic acetylcholine receptor agonist attenuates ILC2-dependent airway hyperreactivity

Lauriane Galle-Treger, Yuzo Suzuki, Nisheel Patel, Ishwarya Sankaranarayanan, Jennifer L. Aron, Hadi Maazi, Lin Chen and Omid Akbari ()
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Lauriane Galle-Treger: Keck School of Medicine, University of Southern California
Yuzo Suzuki: Keck School of Medicine, University of Southern California
Nisheel Patel: Keck School of Medicine, University of Southern California
Ishwarya Sankaranarayanan: Keck School of Medicine, University of Southern California
Jennifer L. Aron: Keck School of Medicine, University of Southern California
Hadi Maazi: Keck School of Medicine, University of Southern California
Lin Chen: University of Southern California
Omid Akbari: Keck School of Medicine, University of Southern California

Nature Communications, 2016, vol. 7, issue 1, 1-13

Abstract: Abstract Allergic asthma is a complex and chronic inflammatory disorder that is associated with airway hyperreactivity (AHR) and driven by Th2 cytokine secretion. Type 2 innate lymphoid cells (ILC2s) produce large amounts of Th2 cytokines and contribute to the development of AHR. Here, we show that ILC2s express the α7-nicotinic acetylcholine receptor (α7nAChR), which is thought to have an anti-inflammatory role in several inflammatory diseases. We show that engagement of a specific agonist with α7nAChR on ILC2s reduces ILC2 effector function and represses ILC2-dependent AHR, while decreasing expression of ILC2 key transcription factor GATA-3 and critical inflammatory modulator NF-κB, and reducing phosphorylation of upstream kinase IKKα/β. Additionally, the specific α7nAChR agonist reduces cytokine production and AHR in a humanized ILC2 mouse model. Collectively, our data suggest that α7nAChR expressed by ILC2s is a potential therapeutic target for the treatment of ILC2-mediated asthma.

Date: 2016
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DOI: 10.1038/ncomms13202

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