Copyright: ©Author(s) 2026. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution-NonCommercial (CC BY-NC 4.0) license. No commercial re-use. See permissions. Published by Baishideng Publishing Group Inc.
World J Gastroenterol. Oct 21, 2026; 32(39): 121041
Published online Oct 21, 2026. doi: 10.3748/wjg.121041
Published online Oct 21, 2026. doi: 10.3748/wjg.121041
Gut microbial metabolites as key mediators in inflammatory bowel disease
Tatiana Sall, Department of Molecular Biology, Genetics and Fundamental Medicine, Institute of Experimental Medicine, St. Petersburg 197022, Russia
Ekaterina Litvinova, Physical Engineering Faculty, Novosibirsk State Technical University, Novosibirsk 630073, Russia
Elena Arzhanova, Faculty of Natural Sciences, Novosibirsk State University, Novosibirsk 630090, Russia
Stanislav Sitkin, Functional Metabolomics and Human Microbiome Research Group, Institute of Perinatology and Pediatrics, Almazov National Medical Research Centre, St. Petersburg 197341, Russia
Stanislav Sitkin, Department of Internal Diseases, Gastroenterology and Dietetics, North-Western State Medical University Named After I.I. Mechnikov, St. Petersburg 191015, Russia
Stanislav Sitkin, Department of Molecular Microbiology, Institute of Experimental Medicine, St. Petersburg 197022, Russia
Timur Vakhitov, Faculty of Biotechnologies, ITMO University, St. Petersburg 197101, Russia
Author contributions: Sall T contributed to the conception, review of literature, and drafting of the manuscript; Sall T, Litvinova E, and Arzhanova E were involved in data collection and analysis; Sitkin S and Vakhitov T designed and supervised this study and guided the revision of the article. All authors contributed to the writing and editing of the manuscript, reviewed and approved the final version of the manuscript.
Supported by Russian Science Foundation, No. 20-65-47026.
Institutional animal care and use committee statement: This study involves animal subjects and was approved by the local Ethics Committee of the Research Institute of Neuroscience and Medicine, Novosibirsk, Russia.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
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: Data can be obtained from the corresponding author.
Corresponding author: Stanislav Sitkin, MD, PhD, Associate Professor, Head, Senior Resear
Received: March 17, 2026
Revised: April 17, 2026
Accepted: June 9, 2026
Published online: October 21, 2026
Processing time: 173 Days and 14.3 Hours
Revised: April 17, 2026
Accepted: June 9, 2026
Published online: October 21, 2026
Processing time: 173 Days and 14.3 Hours
Core Tip
Core Tip: Gut microbial dysbiosis is a driving factor in inflammatory bowel disease (IBD) pathogenesis, mainly through a reduced capacity of the dysbiotic microbiota to synthesize beneficial metabolites, such as short-chain fatty acids, or through increased production of pathogenic metabolites, such as hydrogen sulfide, reactive nitrogen species, and lactate. We found elevated levels of 2-hydroxybutyric acid in Muc2-/- mice’s blood and revealed its ability to worsen IBD progression in the models of the disease. Butyric, propionic, and valeric acids, especially when used in combination, had a therapeutic effect in IBD through their anti-inflammatory and immunomodulatory potential and their gut microbiota-restoring properties.