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Nicotinic acetylcholine receptor agonist attenuates ILC2-dependent airway hyperreactivity

Author

Listed:
  • 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)

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.

Suggested Citation

  • Lauriane Galle-Treger & Yuzo Suzuki & Nisheel Patel & Ishwarya Sankaranarayanan & Jennifer L. Aron & Hadi Maazi & Lin Chen & Omid Akbari, 2016. "Nicotinic acetylcholine receptor agonist attenuates ILC2-dependent airway hyperreactivity," Nature Communications, Nature, vol. 7(1), pages 1-13, December.
    • Handle: RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms13202
    DOI: 10.1038/ncomms13202
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    Cited by:

    1. Jongho Ham & Jihyun Kim & Kyoung-Hee Sohn & In-Won Park & Byoung-Whui Choi & Doo Hyun Chung & Sang-Heon Cho & Hye Ryun Kang & Jae-Woo Jung & Hye Young Kim, 2022. "Cigarette smoke aggravates asthma by inducing memory-like type 3 innate lymphoid cells," Nature Communications, Nature, vol. 13(1), pages 1-12, December.
    2. Emily Howard & Benjamin P. Hurrell & Doumet Georges Helou & Pedram Shafiei-Jahani & Spyridon Hasiakos & Jacob Painter & Sonal Srikanth & Yousang Gwack & Omid Akbari, 2023. "Orai inhibition modulates pulmonary ILC2 metabolism and alleviates airway hyperreactivity in murine and humanized models," Nature Communications, Nature, vol. 14(1), pages 1-13, December.

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