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. 2023 Oct 5;20:224. doi: 10.1186/s12985-023-02194-w

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© The Author(s) 2023

Open Access This 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 — ROS-dependent NET release and NETosis by RSV-infected neutrophils. RSV F glycoprotein stimulates TLR4 which may activate the Raf/MEK/ERK pathway and subsequent NADPH oxidase complexes, leading to ROS production. ROS can promote the separation and loss of the nuclear membrane and activate PAD4-mediated histone citrullination to allow chromatin decondensation. RIPK1/RIPK3/MLKL induces cytomembrane rupture and contributes to NETosis. PI3K/AKT and p38 MAPK are also involved in NETosis, although the mechanism is not fully understood