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World J Gastroenterol. Aug 14, 2026; 32(30): 118010
Published online Aug 14, 2026. doi: 10.3748/wjg.118010
Letter to the Editor: Microbial metabolites and immune regulation in inflammatory bowel disease and metabolic dysfunction-associated steatotic liver disease
Zi-Ke Chen, Min Shi, Yuan-Bin Wu, Jia-Wei Zhao, Yu-Gang Wang
Zi-Ke Chen, Min Shi, Jia-Wei Zhao, Yu-Gang Wang, Department of Gastroenterology, Shanghai Tongren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200336, China
Zi-Ke Chen, Min Shi, Jia-Wei Zhao, Yu-Gang Wang, Hongqiao International Institute of Medicine, Shanghai Tongren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200336, China
Zi-Ke Chen, Min Shi, Jia-Wei Zhao, Yu-Gang Wang, Key Laboratory for Translational Research and Innovative Therapeutics of Gastrointestinal Oncology, Shanghai Tongren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200336, China
Yuan-Bin Wu, Department of Emergency Medicine, The Seventh Medical Center, Chinese PLA General Hospital, Beijing 100700, China
Co-first authors: Zi-Ke Chen and Min Shi.
Co-corresponding authors: Jia-Wei Zhao and Yu-Gang Wang.
Author contributions: Chen ZK and Shi M wrote the original draft as co-first authors; Wu YB assisted in manuscript writing, literature retrieval and literature collection; Zhao JW and Wang YG conceived the article and revised the final draft as the co-corresponding authors; all of the authors read and approved the final version of the manuscript to be published.
AI contribution statement: ChatGPT is only used for language polishing, grammar correction, translation assistance, and improving readability. The entire or any part of the main content (abstract, introduction, materials and methods, results, discussion, and conclusion) of this manuscript is not generated by artificial intelligence. The main scientific content of this paper was written, reviewed, and finalized by the author themselves.
Conflict-of-interest statement: The authors report no relevant conflicts of interest for this article.
Corresponding author: Yu-Gang Wang, MD, PhD, Department of Gastroenterology, Shanghai Tongren Hospital, Shanghai Jiao Tong University School of Medicine, No. 1111 Xianxia Road, Shanghai 200336, China. wang_yugang@sina.com
Received: December 23, 2025
Revised: January 27, 2026
Accepted: February 28, 2026
Published online: August 14, 2026
Processing time: 214 Days and 13 Hours
Abstract

This letter aims to engage in a constructive discussion of the review written by Sokal-Dembowska et al, published in the recent issue of the World Journal of Gastroenterology. The review systematically expounds the role of the gut microbiota in linking inflammatory bowel disease with metabolic dysfunction-associated steatotic liver disease. We commend the authors for integrating evidence on gut dysbiosis, barrier dysfunction, oxidative stress, and the gut-liver axis. Based on this, we further focus on two key aspects: first, the functional impact of metabolites derived from gut microbiota; second, the complex heterogeneity reflected in the balance between T helper cell 17 and regulatory T cells. Additionally, we explore the potential and challenges of targeting the interleukin (IL)-17/IL-23 axis for treatment. To more intuitively illustrate the complex interactions mentioned above, we provide a schematic diagram of immune-metabolic crosstalk. Finally, this article further discusses the clinical significance of these understandings for the development of precise treatment strategies.

Keywords: Gut-liver axis; Metabolic dysfunction-associated steatotic liver disease; Inflammatory bowel disease; Gut microbiota; Th17-regulatory T cell balance

Core Tip: This letter builds on the important review by Sokal-Dembowska et al and further emphasizes the necessity to delve into the functional consequences of alterations in the microbial metabolome, as well as the complexity of Th17/Treg immune regulation in the gut-liver axis between inflammatory bowel disease and metabolic dysfunction-associated steatotic liver disease. Specifically, this article focuses on elaborating how metabolites from specific gut microbiota and pathogenic Th17 cell subsets promote liver damage, and further discusses the translational medical significance of novel interleukin-23 targeted therapeutic strategies and sphingosine-1-phosphate receptor modulators.

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