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. 2021 May 22;18:19. doi: 10.1186/s12950-021-00286-4

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© The Author(s) 2021

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. 6 — Cigarette smoke extract (CS) induced AIM2 inflammasome activation in non-COPD non-smoker control BAL derived alveolar macrophages. a, b Representative confocal images of AIM2 (red, Ab #1, aa250–300/354) and cleaved IL-1β (green) in alveolar macrophages exposed to cigarette smoke extract (B), vs. vehicle control (a). c, d Quantitation of AIM2 and cleaved IL-1β specks (PPC, number of particles per cell) in cells treated with cigarette smoke extract (CSE) vs. vehicle control for paired analysis (n = 8). e Colocalization of cleaved IL-1β with ASC in CSE-treated alveolar macrophages