Skip to content
DraconiticResearch
Search Sources API
197,688 studies31 sourcesUpdated 21 min ago
Peer-reviewedCC BY 4.0International Journal of Molecular Sciences

Short-Chain Fatty Acids as Modulators of the Gut–Immune Axis in Inflammatory Bowel Disease: Linking Metabolism, Immune Regulation, and Epithelial Barrier Function

  1. 1Chair and Department of Conservative Dentistry with Endodontics, Medical University of Lublin, 20-093 Lublin, Poland
  2. 2Faculty of Health Sciences and Psychology, Collegium Medicum, University of Rzeszów, 35-959 Rzeszów, Poland
  3. 3University Center for Research and Development in Health Sciences, University of Rzeszów, 35-959 Rzeszów, Poland

Abstract

Inflammatory bowel diseases (IBDs), which include Crohn’s disease (CD) and ulcerative colitis (UC), are chronic conditions associated with abnormalities in the immune response, gut microbiota dysbiosis, and disruption of the intestinal barrier homeostasis. A growing body of evidence suggests that the gut–immune axis plays a key role in the pathogenesis of IBD, and that metabolites of microbial origin influence the regulation of the immune response and the maintenance of intestinal barrier integrity. Particular importance is attributed to short-chain fatty acids (SCFAs), such as acetate, propionate, and butyrate. The aim of this review is to present the current knowledge regarding the role of SCFAs as modulators of the gut–immune axis in IBD, with particular emphasis on their mechanisms of action and therapeutic potential. Physiologically, SCFAs are produced through the fermentation of dietary fiber by the gut microbiota. However, in IBD, the composition of the gut microbiota is often disrupted. SCFAs influence the expression of inflammatory genes and regulate the function of immune cells. Furthermore, butyrate in particular strengthens the integrity of the intestinal barrier by improving the function of tight junctions (TJs), increasing mucus production, and supporting epithelial regeneration. SCFAs represent an important link between diet, the gut microbiota, and immunity. Strategies to increase their availability may represent a promising approach to supporting IBD treatment, but they require further evaluation in well-designed clinical trials involving humans.

Related

  1. Sialic acid cis-ligands as modulators of Siglec function in cancer immunity
    Anne H.C. Valk, Matthia G.M. Boros, Fabian Schuurmans +2
    OncoimmunologyPeer-reviewedCC BY-NC 4.0Full textMolecular biology & gene regulationPMC
  2. Roles of proprotein convertase subtilisin/kexin type 9 (PCSK9) in the regulation of hepatic triglyceride metabolism
    Journal of lipid researchPeer-reviewedCC BYFull textEnzymology & metabolismEurope PMC
  3. AbaI/AbaR Quorum Sensing in Acinetobacter baumannii: Virulence Regulation, Epithelial Injury, Innate Immune Activation and Anti-Virulence Strategies
    Tomasz Busłowicz, Karolina Pawłuszkiewicz, Zofia Biel +5
    International Journal of Molecular SciencesPeer-reviewedCC BY 4.0Full textMolecular biology & gene regulationCrossrefEurope PMC
  4. Progerin disrupts intestinal epithelial homeostasis by impairing mitochondrial metabolism and absorptive enterocyte maturation
    C. Reisacher, M. Singh, L. Arbibe
    bioRxivPreprintCC BY-NCFull textMolecular biology & gene regulationbioRxiv
  5. 2-Hydroxyoleic Acid Preserves Lipid Homeostasis and Epithelial Barrier Function in Experimental Colitis
    Lin Lin, Jianyu Zhu, Yibin Ren +1
    Journal of Lipid ResearchPeer-reviewedCC BY 4.0Enzymology & metabolismCrossref
BibTeX
@article{piatek2026shortchain,
  title = {{Short-Chain Fatty Acids as Modulators of the Gut–Immune Axis in Inflammatory Bowel Disease: Linking Metabolism, Immune Regulation, and Epithelial Barrier Function}},
  author = {Dominika Piątek and Aneta Sokal-Dembowska and Małgorzata Strycharz-Dudziak and Sara Jarmakiewicz-Czaja},
  journal = {International Journal of Molecular Sciences},
  year = {2026},
  month = oct,
  doi = {10.3390/ijms27219710},
  url = {https://www.mdpi.com/1422-0067/27/21/9710},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Short-Chain Fatty Acids as Modulators of the Gut–Immune Axis in Inflammatory Bowel Disease: Linking Metabolism, Immune Regulation, and Epithelial Barrier Function
AU  - Dominika Piątek
AU  - Aneta Sokal-Dembowska
AU  - Małgorzata Strycharz-Dudziak
AU  - Sara Jarmakiewicz-Czaja
PY  - 2026
DA  - 2026/10/29
JO  - International Journal of Molecular Sciences
DO  - 10.3390/ijms27219710
UR  - https://www.mdpi.com/1422-0067/27/21/9710
AB  - Inflammatory bowel diseases (IBDs), which include Crohn’s disease (CD) and ulcerative colitis (UC), are chronic conditions associated with abnormalities in the immune response, gut microbiota dysbiosis, and disruption of the intestinal barrier homeostasis. A growing body of evidence suggests that the gut–immune axis plays a key role in the pathogenesis of IBD, and that metabolites of microbial origin influence the regulation of the immune response and the maintenance of intestinal barrier integrity. Particular importance is attributed to short-chain fatty acids (SCFAs), such as acetate, propionate, and butyrate. The aim of this review is to present the current knowledge regarding the role of SCFAs as modulators of the gut–immune axis in IBD, with particular emphasis on their mechanisms of action and therapeutic potential. Physiologically, SCFAs are produced through the fermentation of dietary fiber by the gut microbiota. However, in IBD, the composition of the gut microbiota is often disrupted. SCFAs influence the expression of inflammatory genes and regulate the function of immune cells. Furthermore, butyrate in particular strengthens the integrity of the intestinal barrier by improving the function of tight junctions (TJs), increasing mucus production, and supporting epithelial regeneration. SCFAs represent an important link between diet, the gut microbiota, and immunity. Strategies to increase their availability may represent a promising approach to supporting IBD treatment, but they require further evaluation in well-designed clinical trials involving humans.
SN  - 1422-0067
ER  -