# Research Progress on the Mechanisms of Gut Microbiota Dysbiosis Associated With Idiopathic Pulmonary Fibrosis: A Review

**Authors:** Xiaolong Li, Shuhao Xu, Yi Li, Rongli Wang, Chao Qin, Xin Wang

PMC · DOI: 10.7759/cureus.102429 · Cureus · 2026-01-27

## TL;DR

This review explores how changes in gut bacteria may contribute to the development of idiopathic pulmonary fibrosis and highlights potential treatments targeting the gut-lung connection.

## Contribution

The paper systematically integrates recent findings on gut microbiota dysbiosis and its role in IPF, emphasizing the gut-lung axis and novel therapeutic strategies.

## Key findings

- Gut microbiota alterations are associated with idiopathic pulmonary fibrosis.
- Microbial metabolites and immune modulation are key in linking gut dysbiosis to lung disease.
- Probiotics and fecal microbiota transplantation show potential as therapeutic approaches for IPF.

## Abstract

Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive fibrotic interstitial lung disease with an incompletely understood pathogenesis. In recent years, growing evidence has highlighted the critical role of gut microbiota dysbiosis in the onset and progression of IPF. This review comprehensively summarizes the characteristics of gut microbiota alterations associated with IPF, explores the underlying mechanisms driving these changes, and examines their impact on disease development. Particular emphasis is placed on the emerging concept of the “gut-lung axis,” which elucidates the bidirectional communication between the intestinal microbiome and pulmonary health. The review further discusses microbial metabolites and immune modulation as key mediators linking gut dysbiosis to pulmonary fibrosis. Additionally, current advances in microbiota-targeted therapeutic strategies, including probiotics, prebiotics, and fecal microbiota transplantation, are analyzed for their potential in IPF management. By systematically integrating recent findings, this article aims to deepen the understanding of IPF pathophysiology and provide a theoretical foundation for novel treatment targets centered on gut microbiota regulation.

## Linked entities

- **Diseases:** idiopathic pulmonary fibrosis (MONDO:0800029), pulmonary fibrosis (MONDO:0002771)

## Full-text entities

- **Genes:** TLR4 (toll like receptor 4) [NCBI Gene 7099] {aka ARMD10, CD284, TLR-4, TOLL}, TLR2 (toll like receptor 2) [NCBI Gene 7097] {aka CD282, TIL4}, FFAR3 (free fatty acid receptor 3) [NCBI Gene 2865] {aka FFA3R, GPR41}, MUC5B (mucin 5B, oligomeric mucus/gel-forming) [NCBI Gene 727897] {aka MG1, MUC-5B, MUC5, MUC9}, AHR (aryl hydrocarbon receptor) [NCBI Gene 196] {aka FVH3, RP85, bHLHe76}, NFKB1 (nuclear factor kappa B subunit 1) [NCBI Gene 4790] {aka CVID12, EBP-1, KBF1, NF-kB, NF-kB1, NF-kappa-B1}, NR1H4 (nuclear receptor subfamily 1 group H member 4) [NCBI Gene 9971] {aka BAR, FXR, HRR-1, HRR1, PFIC5, RIP14}, IL17A (interleukin 17A) [NCBI Gene 3605] {aka CTLA-8, CTLA8, IL-17, IL-17A, IL17, ILA17}, Tgfb1 (transforming growth factor, beta 1) [NCBI Gene 21803] {aka TGF-beta1, TGFbeta1, Tgfb, Tgfb-1}, TGFB1 (transforming growth factor beta 1) [NCBI Gene 7040] {aka CAEND1, CED, DPD1, IBDIMDE, LAP, TGF-beta1}, GPBAR1 (G protein-coupled bile acid receptor 1) [NCBI Gene 151306] {aka BG37, GPCR19, GPR131, M-BAR, TGR5}, FFAR2 (free fatty acid receptor 2) [NCBI Gene 2867] {aka FFA2R, GPR43}
- **Diseases:** fibrosis (MESH:D005355), GERD (MESH:D005764), respiratory infections (MESH:D012141), inflammation (MESH:D007249), respiratory diseases (MESH:D012140), Dysbiosis (MESH:D064806), fibrotic lung diseases (MESH:D008171), lung tissue injury (MESH:D055370), lung inflammation (MESH:D011014), metabolic disorders (MESH:D008659), endotoxemia (MESH:D019446), malnutrition (MESH:D044342), immune (MESH:D007154), IPF (MESH:D054990), cardiovascular disease (MESH:D002318), pulmonary fibrosis (MESH:D011658), systemic (MESH:D015619), interstitial lung disease (MESH:D017563), immune dysregulation (OMIM:614878), tissue injury (MESH:D017695)
- **Chemicals:** palmitoylethanolamide (MESH:C005958), trimethylamine-N-oxide (MESH:C005855), pectin (MESH:D010368), bleomycin (MESH:D001761), inulin (MESH:D007444), bile acid (MESH:D001647), LP03 (-), amino acid (MESH:D000596), butyrate (MESH:D002087), pirfenidone (MESH:C093844), xylooligosaccharides (MESH:C570991), propionate (MESH:D011422), Prebiotics (MESH:D056692), lipid (MESH:D008055), tryptophan (MESH:D014364), acetate (MESH:D000085), SCFA (MESH:D005232), nintedanib (MESH:C530716)
- **Species:** Lactiplantibacillus sp. (species) [taxon 2767846], Escherichia coli (E. coli, species) [taxon 562], Mus musculus (house mouse, species) [taxon 10090], Bifidobacteriales (order) [taxon 85004], Prevotella (genus) [taxon 838], Roseburia (genus) [taxon 841], Ruminococcus (genus) [taxon 1263], Enterobacterales (order) [taxon 91347], Bacteria Latreille et al. 1825 (Bacteria stick insect, genus) [taxon 629395], Clostridioides difficile (species) [taxon 1496], Homo sapiens (human, species) [taxon 9606], Faecalibacterium prausnitzii (species) [taxon 853], Enterobacteriaceae (enterobacteria, family) [taxon 543], Bacillota (clostridial firmicutes, phylum) [taxon 1239]

## Full text

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## References

22 references — full list in the complete paper: https://tomesphere.com/paper/PMC12945460/full.md

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Source: https://tomesphere.com/paper/PMC12945460