Observational Study
Copyright ©The Author(s) 2021. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastrointest Surg. Nov 27, 2021; 13(11): 1448-1462
Published online Nov 27, 2021. doi: 10.4240/wjgs.v13.i11.1448
Novel roles of lipopolysaccharide and TLR4/NF-κB signaling pathway in inflammatory response to liver injury in Budd-Chiari syndrome
Jie Li, Xiao-Ming Chen, Chun-Ze Zhou, Wei-Wei Fang, Wei-Fu Lv, De-Lei Cheng
Jie Li, Chun-Ze Zhou, Wei-Fu Lv, De-Lei Cheng, Department of Interventional Radiology, The First Affiliated Hospital of University of Science and Technology of China, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei 230001, Anhui Province, China
Xiao-Ming Chen, Department of Gastroenterology, The Second Hospital of Anhui Medical University, Hefei 230000, Anhui Province, China
Wei-Wei Fang, Department of Radiology, The Third People’s Hospital of Hefei, Hefei 230022, Anhui Province, China
Author contributions: Cheng DL and Lv WF designed the study; Li J, Cheng DL, Zhou CZ, Chen ZM and Fang WW performed the experiments, collected and analyzed the data; Lv WF, Zhou CZ, Chen XM and Fang WW contributed to sample collection and experimental data input into computer; Li J and Cheng DL drafted and wrote the manuscript; Li J and Cheng DL gave advice on the experimental design, interpreted the results and critically revised the manuscript; Lv WF, Zhou CZ and Chen XM provided pathological assistance; all authors read and approved the final version of the manuscript.
Supported by Natural Science Foundation Project of Anhui Province, No. 1708085QH218.
Institutional review board statement: All procedures were performed in accordance with the ethical standards of the committee of human experimentation (institutional and national) and with the guidelines of the Helsinki Declaration of 1975 that have been revised in 2008 (5).
Informed consent statement: All study participants, or their legal guardian, provided informed written consent prior to study enrollment.
Conflict-of-interest statement: The authors declare no conflicts of interest.
Data sharing statement: Data are available on reasonable request from the corresponding author.
STROBE statement: The authors have read the STROBE Statement-checklist of items, and the manuscript was prepared and revised according to the STROBE Statement-checklist of items.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: De-Lei Cheng, Department of Interventional Radiology, The First Affiliated Hospital of University of Science and Technology of China, Division of Life Sciences and Medicine, University of Science and Technology of China, No. 218 Jixi Road, Hefei 230001, Anhui Province, China. 39055004@qq.com
Received: January 13, 2021
Peer-review started: January 13, 2021
First decision: July 14, 2021
Revised: August 19, 2021
Accepted: October 31, 2021
Article in press: October 31, 2021
Published online: November 27, 2021
Processing time: 317 Days and 14.4 Hours
Core Tip

Core Tip: Budd-Chiari syndrome (BCS) is an uncommon disorder characterized by obstruction of hepatic venous outflow. When the liver becomes congested and damaged, liver fibrosis and cirrhosis can occur. We explored the mechanism involving NF-κB in BCS-induced liver injury in humans and animal models. Results suggest that LPS level is markedly elevated in BCS, and in turn it activates the TLR4/NF-κB signaling pathway, leading to induction of inflammatory cytokines (tumor necrosis factor-α, interleukin-2 and interferon-γ) in response to BCS-induced liver injury. Importantly, our novel findings indicated that the TLR4/NF-κB signaling pathway could be a potential therapeutic target.