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. 2021 Jun 11;12(6):606. doi: 10.1038/s41419-021-03896-1

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© The Author(s) 2021

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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 8 — In the case of sepsis, increased neutrophils migrate and aggregate in the intestine and trigger NETosis. Excessive NETs formation can activate the TLR9–ER stress–ROS signaling pathway, which enhances intestinal epithelial cell apoptosis and the inflammatory response. Uncontrolled intestinal epithelial cell injury results in intestinal barrier disruption, leading to bacterial translocation.