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. 2021 Jun 7;18:120. doi: 10.1186/s12985-021-01578-0

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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. 2 — SARS-CoV-2 enters alveolar cells via ACE2 receptor. Initially, epithelial cells infected by SARS viruses act as a

source of cytokines, releasing interleukin-1, interleukin-6, interleukin-8 and several other chemokines that can activate macrophages, attract neutrophils cause homing of monocytes and macrophages to sites of inflammation. After generating initial inflammatory response to alveolar damage, monocytes and macrophages are believed to contribute to production of cytokines. Thus, SARS-CoV triggers macrophages to increase production of certain chemokines (for example, MIP1α), and TNF and interleukin-6. This further activates neutrophils and macrophages which infiltrate the alveoli and cause tissue destruction [81]. (Image created with Biorender.com)