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. 2021 May 31;19:162. doi: 10.1186/s12951-021-00909-1

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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. 9 — Loss of lc3b aggravated pulmonary inflammation induced by CuONPs. Wild type and lc3b^-/- mice were intratracheally instilled of vehicle or 5 mg/kg CuONPs, respectively, then the lung tissues of indicated groups were collected 3 days after treatment. The mRNA expression levels of A Il-1β, B Il-6 and C Tnf-α in mice lung tissues in the indicated groups were determined by QPCR analysis. D The expression levels of CD68 in mice lung tissues in the indicated groups were determined by IHC analysis. Scale bar, 100 μm in the upper panels and 50 μm in the bottom panels. E The average of CD68 intensity shown in (D) were quantified. F The mRNA expression levels of Ccl2 and Sele in mice lung tissues in the indicated groups were determined by QPCR analysis. *indicates p < 0.05 compared with indicated group