ArticleThe clinical respiratory journal2025
The Role of Gut Microbiota on Idiopathic Pulmonary Fibrosis Mediated by Circulating Inflammatory Proteins: A Two-Step, Two-Sample Mendelian Randomization Study.
Article in The clinical respiratory journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Most Promising Emerging Therapies for Pulmonary Fibrosis: Targeting Novel Pathways.Biomedicines · 2026Review
- Exploring microbial signatures in sarcoidosis: etiological and therapeutic implications of host-microbiota interactions.Frontiers in immunology · 2026Review
- The Role of Gut Microbiota on Idiopathic Pulmonary Fibrosis Mediated by Circulating Inflammatory Proteins: A Two-Step, Two-Sample Mendelian Randomization Study.The clinical respiratory journal · 2025Article
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPersistent inflammation is a crucial characteristic of idiopathic pulmonary fibrosis (IPF). Gut microbiota (GM) contribute to the occurrence and development of several pulmonary diseases through the "gut-lung axis." The genetic role of GM in IPF and the mediating effect of circulating inflammatory proteins.
methodsA single nucleotide polymorphism (SNP) was used as an instrumental variable (IV) for exposure to evaluate the causal relationship between exposure and outcome. A two-step, two-sample Mendelian randomization study mainly based on an "inverse variance weighted (IVW)" approach was performed to explore the causal relationship between GM and IPF mediated by circulating inflammatory proteins.
resultsThe IVW way illustrated 12 taxa (Bacillales, Gastranaerophilales, Selenomonadales, Family XIII, Bacteroidaceae, Bacteroides, and Actinomyces, Bifidobacterium, Oscillibacter, Ruminococcus gnavus, Subdoligranulum, Veillonella) of GM and 8 circulating inflammatory proteins (CCL11, CXCL6, CXCL9, CCL8, CCL7, NRTN, STAMPB, and TGFa) had suggestive evidence of causality on IPF. The mediation MR demonstrated the causal pathway from Actinomyces to IPF was partly mediated by CCL11 (the mediation effect: 0.063, 95% CI [1.016-1.126]; p = 0.004) with a mediation proportion of 13.035%.
conclusionsThese findings may suggest a genetically predicted association between GM and IPF mediated by circulating inflammatory proteins.
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