Evidence map›Paper›PMID 41965517›Full record

ArticleBMC microbiology2026

Intestinal dysbiosis associates with silica-induced pulmonary fibrosis in mice via arginine and tryptophan pathways.

Jie Han, Xinyu Zhou, Mingliang Guo, Chongyang Zhang, Chuncheng Liu, Lu Cai, Hongyu Zhao

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in BMC microbiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Jie Han *Inner Mongolia Key Laboratory of Life Health and Bioinformatics, School of Life Science and Technology, Inner Mongolia University of Science and Technology, Baotou, 014010, China.
Xinyu Zhou *Inner Mongolia Key Laboratory of Life Health and Bioinformatics, School of Life Science and Technology, Inner Mongolia University of Science and Technology, Baotou, 014010, China.ORCID 0000-0002-4230-8279
Mingliang GuoInner Mongolia Key Laboratory of Life Health and Bioinformatics, School of Life Science and Technology, Inner Mongolia University of Science and Technology, Baotou, 014010, China.
Chongyang ZhangInner Mongolia Key Laboratory of Life Health and Bioinformatics, School of Life Science and Technology, Inner Mongolia University of Science and Technology, Baotou, 014010, China.
Chuncheng LiuInner Mongolia Key Laboratory of Life Health and Bioinformatics, School of Life Science and Technology, Inner Mongolia University of Science and Technology, Baotou, 014010, China.
Lu CaiInner Mongolia Key Laboratory of Life Health and Bioinformatics, School of Life Science and Technology, Inner Mongolia University of Science and Technology, Baotou, 014010, China.
Hongyu ZhaoInner Mongolia Key Laboratory of Life Health and Bioinformatics, School of Life Science and Technology, Inner Mongolia University of Science and Technology, Baotou, 014010, China. zhaohongyu2000@163.com.ORCID 0000-0003-1477-5731

Funding

National Natural Science Foundation of China 62231013National Natural Science Foundation of China 62261043Natural Science Foundation of Inner Mongolia 2025MS03093Natural Science Foundation of Inner Mongolia 2025QN03136
6 · The paper itself

Abstract

backgroundPulmonary fibrosis (PF) is a life-threatening interstitial lung disease with a lack of effective therapeutic approaches. Silicosis is a subtype of PF that is specifically caused by the inhalation of crystalline silica particles. In recent years, the gut-lung axis has been shown to be involved in the occurrence and progression of various respiratory diseases. However, the involvement and specific mechanism of action of the gut microbiome in silica-induced PF remain to be elucidated. Therefore, we established a silica-induced PF murine model using an inhalation exposure system, and combined gut metagenomic and untargeted metabolomics data to correlate microbial and metabolic changes with profibrotic cytokine levels.

resultsIn mice exposed to silica dust for 64 days and 128 days, Akkermansia muciniphila and Staphylococcus lentus were significantly enriched, whereas the abundance of Lactobacillus murinus was notably reduced. Relevant network analysis revealed that these gut microbiota changes were highly correlated with metabolic disorders of tryptophan and arginine. Moreover, changes in the gut microbiome composition corresponded with the fluctuations in the levels of profibrotic cytokines, including transforming growth factor-beta, tumor necrosis factor-alpha, fibroblast growth factor, and hydroxyproline.

conclusionWe successfully established a murine model of PF induced by silica inhalation. Our results suggest that Lactobacillus murinus, Akkermansia muciniphila, and Staphylococcus lentus are key microorganisms involved in the development of silica-induced PF, while the arginine and tryptophan metabolic pathways serve as key regulatory pathways in the gut-lung axis contributing to disease development.

Indexed as

ArginineDysbiosisGastrointestinal MicrobiomePulmonary FibrosisSilicon DioxideTryptophanAkkermansiaAnimalsCytokinesDisease Models, AnimalLungMaleMiceMice, Inbred C57BLArginineCytokinesSilicon DioxideTryptophanAmino acid metabolismPulmonary fibrosisRegulatory networkSilicosisUntargeted metabolomics

Identifiers

PMID41965517
PMCPMC13214178

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.