Basic Study
Copyright ©The Author(s) 2025. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Jun 14, 2025; 31(22): 108815
Published online Jun 14, 2025. doi: 10.3748/wjg.v31.i22.108815
Intermittent fasting exacerbates colon inflammation by promoting Th17 cell differentiation through inhibition of gut microbiota-derived indoleacrylic acid
Rui Fu, Peng Zhang, Jia-Wei Zhang, Yuan Hong, Bo Chen, Guo-Dong Cao
Rui Fu, Peng Zhang, Jia-Wei Zhang, Yuan Hong, Bo Chen, Guo-Dong Cao, Department of General Surgery, The First Affiliated Hospital of Anhui Medical University, Hefei 230022, Anhui Province, China.
Co-first authors: Rui Fu and Peng Zhang.
Co-corresponding authors: Bo Chen and Guo-Dong Cao.
Author contributions: Fu R contributed to project administration, visualization, experimental operation; Zhang P contributed to data curation, writing original draft; Zhang JW contributed to formal analysis, methodology; Hong Y contributed to resources, polish the article; Chen B contributed to funding acquisition, writing review and editing; Cao GD contributed to funding acquisition, supervision, writing review and editing.
Supported by the Anhui University Research Project, No. 2022AH051171; Natural Science Foundation Project of Anhui Province, No. 2408085QH271; Anhui Medical University Scientific Research Level Improvement Plan, No. 2022xkjT028; Health Research Project of Anhui Province, No. AHWJ2023A30047; the Anhui Provincial Natural Science Foundation, No. 2208085MH240; the Scientific Research Project of Anhui Provincial Department of Education, No. 2022AH051167; the Anhui Quality Engineering Project, No. 2023sx200, No. 2023jyjxggyjY087 and No. 2023zyxwjxalk046; the Anhui Provincial Postgraduate Education Quality Project, No. 2024cxcysj062; and Anhui Medical University Graduate Research and Practice Innovation Project, No. YJS20240095.
Institutional review board statement: This study does not involve any human experiments.
Institutional animal care and use committee statement: All procedures involving animals were reviewed and approved by the Institutional Animal Care and Use Committee of the Anhui Medical University (No. LLSC20242418).
Conflict-of-interest statement: The authors declare that they have no conflict of interest.
ARRIVE guidelines statement: The authors have read the ARRIVE guidelines, and the manuscript was prepared and revised according to the ARRIVE guidelines.
Data sharing statement: Technical appendix, statistical code, and dataset available from the corresponding author at 11718242@zju.edu.cn. Consent was not obtained but the presented data are anonymized and risk of identification is low. The 16S rRNA gene sequencing data (accession number: PRJNA1259772), transcriptomic data (accession number: PRJNA1260448), and multi-omics dataset related to Th17 cell differentiation (accession number: OMIX010115) are publicly available.
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: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Guo-Dong Cao, MD, PhD, Doctor, Associate Professor, Department of General Surgery, The First Affiliated Hospital of Anhui Medical University, No. 218 Jixi Road, Hefei 230022, Anhui Province, China. 11718242@zju.edu.cn
Received: April 27, 2025
Revised: May 10, 2025
Accepted: May 26, 2025
Published online: June 14, 2025
Processing time: 49 Days and 14.2 Hours
Core Tip

Core Tip: This study demonstrates that long-term intermittent fasting (IF) compromises intestinal barrier function, alters the metabolite profile (reducing anti-inflammatory compounds and increasing pro-inflammatory ones), and induces dysbiosis (increasing pathogenic bacteria while decreasing short-chain fatty acid-producing bacteria), which collectively promote Th17-driven inflammation. Exogenous indoleacrylic acid supplementation restores barrier integrity, suppresses Th17 activation, and enhances interleukin-10 expression, highlighting its therapeutic promise and emphasizing the need for a reevaluation of the long-term safety of IF due to its potential gut-disrupting effects.