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Critical role of interleukin-23 in development of asthma promoted by cigarette smoke

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A Correction to this article was published on 22 May 2019

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Abstract

It has been recently reported that cigarette smoke exposure during allergen sensitization facilitates the development of allergic asthma; however, the underlying mechanisms remain elusive. We evaluated the role of interleukin (IL-23) in a cigarette smoke extract (CSE)-induced Dermatophagoides pteronyssinus (Dp)-allergic asthma mouse model. BALB/c mice were exposed to CSE during allergen sensitization period. Anti-IL-23p19 or IL-23R antibody was administered during the sensitization period. And we evaluated several immunological responses. The expression of IL-23 and IL-23 receptor (IL-23R) was examined in lung tissue. IL-23 and IL-23R expression was increased in the airway epithelium of Dp/CSE co-administered mice. CSE administration during the sensitization promoted Dp-allergic sensitization and the development of asthma phenotypes. Additionally, the proportion of innate lymphoid type 2 cells (ILC2) was also increased by CSE and Dp co-instillation. Anti-IL-23 or IL-23R antibody treatment during allergen sensitization significantly diminished phenotypes of allergic asthma and the ILC2 population. The levels of IL-33 and thymic stromal lymphopoietin (TSLP) were also significantly reduced by anti-IL-23 or IL-23R antibody treatment. IL-23 may thus play a significant role in cigarette smoke-induced allergic sensitization and asthma development. Clinically, the increase in allergen sensitization due to cigarette exposure causes onset of asthma, and IL-23 may be important in this mechanism.

Key messages

  • IL-23 and IL-23R expression was increased in the lung epithelium of Dp and CSE co-exposed mice during sensitization period.

  • The population of ILC2s was increased in Dp and CSE co-exposed mice during sensitization period.

  • Anti-IL23 or IL-23R antibody treatment with co-administration of CSE and HDM during sensitization period significantly suppresses ILC2.

  • In vitro, IL-23 blockade in Dp and CSE-stimulated epithelial cells suppressed IL-13 expression in ILC2.

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  • 22 May 2019

    The original publication of this paper contains a mistake.

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Acknowledgements

We thank Hee-seung Lee for her comments on this manuscript.

Funding

This work was supported by the National Research Foundation of Korea (NRF) grant funded by the Korea government (MSIT) (NRF-2016R1C1B1010632).

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Correspondence to Hyun Seung Lee.

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All experiments were performed with the approval of the Institutional Animal Care and Use Committee of the Institute (IACUC) of Seoul National University. The approval number is SNU-160615-5-4.

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The original version of this article was revised: The original publication of this paper contains a mistake. Correct images for figures 1,2, 3, 4 and 5 are shown in this paper.

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Lee, H.S., Park, DE., Lee, JW. et al. Critical role of interleukin-23 in development of asthma promoted by cigarette smoke. J Mol Med 97, 937–949 (2019). https://doi.org/10.1007/s00109-019-01768-y

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  • DOI: https://doi.org/10.1007/s00109-019-01768-y

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