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. 2020 Apr 22;21:95. doi: 10.1186/s12931-020-01358-4

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© The Author(s) 2020

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 3 — ALT inhibited CSE induced - IL-1 β, TNF-α, IL-6 and IFN-γ production in Beas-2B and NHBE cells. a ALT inhibited CSE induced inflammatory response in Beas-2B cells; b ALT inhibited CSE induced inflammatory response in NHBE cells. Beas-2B and NHBE cells were pre-treated with 1, 5 and 10 μM ALT for 2 h and then administrated with 5% CSE for 24 h. The commercially available ELISA kits were used to measure the level of IL-1 β, TNF-α, IL-6 and IFN-γ. Data were expressed as mean ± S.D. from three independent experiments. ^*P values < 0.05 compared with the control group, ^#P values < 0.05 compared with the CSE group. CSE: cigarette smoke extract; ALT: Alantolactone