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. 2021 Jul 16;9:702890. doi: 10.3389/fcell.2021.702890

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Copyright © 2021 Wang, Zhang, Liu, Xu and Liu.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Proposed mechanism of LSEC barrier in the gut–liver axis. A leaky gut can lead to the translocation of gut-derived pathogenic factors [e.g., lipopolysaccharide (LPS)] to the portal vein and encounter liver sinusoidal endothelial cells (LSECs). Under normal conditions, the intact LSEC barrier can defend against these invasive factors. When LSECs are damaged, they can shift toward a pro-inflammatory phenotype. Under the stimulation of gut-derived LPS, damaged LSECs can secrete pro-inflammatory mediators including neutrophil-chemoattractant CXCL1 and TNF-α. CXCL1 induces the recruitment of peripheral blood neutrophils into the liver. Neutrophils are further activated by gut-derived LPS and LSEC-derived TNF-α. Activated neutrophils can produce massive reactive oxygen species (ROS), pro-inflammatory cytokines, and neutrophil extracellular traps (NETs), which lead to enhanced liver injury.