Evidence map›Paper›PMID 41851729›Full record

ArticleJournal of nanobiotechnology2026

Parabacteroides goldsteinii-derived outer membrane vesicles alleviate acute lung injury via modulation of bile acid metabolism.

Wensi Zhu, Linxiao Han, Ludan He, Shuoyan Wei, Juan Li, Liangcao Xin, Haiyun Zhang, Jie Shen, Yuanlin Song, Jiebai Zhou and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of nanobiotechnology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Review
  2. Article
  3. Journal of inflammation research · 2026
    Article
  4. 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

12 authors.

Wensi Zhu *Department of Pulmonary and Critical Care Medicine, Shanghai Respiratory Research Institute, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
Linxiao Han *Department of Pulmonary and Critical Care Medicine, Shanghai Respiratory Research Institute, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
Ludan He *Shanghai Institute of Infectious Disease and Biosecurity, Fudan University, Shanghai, 200032, China.
Shuoyan Wei *Department of Pulmonary and Critical Care Medicine, Shanghai Respiratory Research Institute, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
Juan LiDepartment of Pulmonary and Critical Care Medicine, Shanghai Respiratory Research Institute, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
Liangcao XinShanghai Institute of Infectious Disease and Biosecurity, Fudan University, Shanghai, 200032, China.
Haiyun ZhangDepartment of Thoracic Surgery, Xiamen Chang Gung Hospital Hua Qiao University, Xiamen Fujian, 361028, China.
Jie ShenCenter of Emergency and Critical Medicine, Jinshan Hospital of Fudan University, Fudan University, Shanghai, 200540, China.
Yuanlin SongDepartment of Pulmonary and Critical Care Medicine, Shanghai Respiratory Research Institute, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
Jiebai ZhouDepartment of Pulmonary and Critical Care Medicine, Shanghai Respiratory Research Institute, Zhongshan Hospital, Fudan University, Shanghai, 200032, China. zhou.jiebai@zs-hospital.sh.cn.
Chih-Jung ChangSchool of Medicine, Hua Qiao University, Quanzhou, 362021, Fujian, China. chihjungchang@hqu.edu.cn.
Jian ZhouDepartment of Pulmonary and Critical Care Medicine, Shanghai Respiratory Research Institute, Zhongshan Hospital, Fudan University, Shanghai, 200032, China. zhou.jian@fudan.edu.cn.

Funding

National Key Research and Development Program of China 2022YFA0806200National Natural Science Foundation of China 82470069Science and Technology Commission of Shanghai Municipality 20DZ2254400Science and Technology Commission of Shanghai Municipality 20DZ2261200Shanghai Jinshan Municipal Health Commission JSZK2019A01Shanghai Municipal Science and Technology Major Project ZD2021CY001
6 · The paper itself

Abstract

backgroundAcute respiratory distress syndrome (ARDS) is a severe clinical syndrome with limited therapeutic options. Acute lung injury (ALI) is widely used as an experimental animal model that recapitulates the key pathological features of human ARDS. Parabacteroides goldsteinii, a newly identified Gram-negative probiotic, exhibits anti-inflammatory effects in certain disease models. Gram-negative bacteria release nanoscale structures called outer membrane vesicles (OMVs), which show varying composition across species. The role of P. goldsteinii-derived OMVs (Pg-OMVs) in ALI or ARDS remains to be elucidated.

resultIn this study, we investigated the therapeutic potential of Pg-OMVs in a bleomycin (BLM)-induced ALI mouse model and explored their effects on pulmonary inflammation and gut microbiota composition. Compared to mice receiving BLM alone, Pg-OMV-treated mice exhibited significantly reduced inflammatory cell infiltration and lower levels of pro-inflammatory cytokines. Notably, Pg-OMV treatment significantly altered the gut microbiota composition, characterized by an increased abundance of Akkermansia muciniphila and a decreased abundance of Clostridia_bacterium. Fecal microbiota transplantation (FMT) experiments confirmed that the protective effects of Pg-OMVs were mediated via gut-lung axis. Further analysis revealed elevated cholic acid (CA) levels in the peripheral blood and bronchoalveolar lavage fluid following Pg-OMV treatment. CA was shown to suppress BLM-induced macrophage pyroptosis in the lung. Pharmacological inhibition of CA reversed the protective effects of Pg-OMVs, further confirming its pivotal role.

conclusionsIn summary, Pg-OMVs increased the abundance of Akkermansia muciniphila while decreasing the abundance of Clostridia_bacterium in the gut, elevated systemic CA levels, and suppressed macrophage pyroptosis via inhibition of the NF-κB pathway, thereby attenuating pulmonary inflammation and ultimately alleviating ALI. These findings highlight a novel therapeutic strategy for the treatment of ALI or ARDS by targeting the gut-lung axis.

Indexed as

Acute Lung InjuryBacterial Outer MembraneBile Acids and SaltsAnimalsBleomycinCytokinesDisease Models, AnimalGastrointestinal MicrobiomeLungMaleMiceMice, Inbred C57BLBile Acids and SaltsBleomycinCytokinesAcute respiratory distress syndromecholic acidouter membrane vesiclesParabacteroides goldsteiniipyroptosis

Identifiers

PMID41851729
PMCPMC13113110

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.