Evidence map›Paper›PMID 40435188›Full record

ArticlePloS one2025

The role of gut leakage and immune cell miss-homing on gut dysbiosis-induced lung inflammation in a DSS mice model.

Mariam Wed Eladham, Narjes Saheb Sharif-Askari, Priyadharshini Sekar, Bushra Mdkhana, Balachandar Selvakumar, Baraa Khalid Salah Al-Sheakly, Fatemeh Saheb Sharif-Askari, Ibrahim Hachim, Rabih Halwani

Abstract read
In one paragraph

Article in PloS one, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. The therapeutic potential ofFrontiers in microbiology · 2026
    Review
  9. Article
  10. Review
  11. 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

9 authors.

Mariam Wed EladhamResearch Institute for Medical and Health Sciences, University of Sharjah, Sharjah, United Arab Emirates.
Narjes Saheb Sharif-AskariResearch Institute for Medical and Health Sciences, University of Sharjah, Sharjah, United Arab Emirates.
Priyadharshini SekarResearch Institute for Medical and Health Sciences, University of Sharjah, Sharjah, United Arab Emirates.
Bushra MdkhanaResearch Institute for Medical and Health Sciences, University of Sharjah, Sharjah, United Arab Emirates.
Balachandar SelvakumarResearch Institute for Medical and Health Sciences, University of Sharjah, Sharjah, United Arab Emirates.
Baraa Khalid Salah Al-SheaklyResearch Institute for Medical and Health Sciences, University of Sharjah, Sharjah, United Arab Emirates.
Fatemeh Saheb Sharif-AskariResearch Institute for Medical and Health Sciences, University of Sharjah, Sharjah, United Arab Emirates.
Ibrahim HachimResearch Institute for Medical and Health Sciences, University of Sharjah, Sharjah, United Arab Emirates.
Rabih HalwaniResearch Institute for Medical and Health Sciences, University of Sharjah, Sharjah, United Arab Emirates.ORCID https://orcid.org/0000-0002-6516-7771

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundInflammatory Bowel Disease (IBD), encompassing Crohn's disease and ulcerative colitis, affects millions globally, with extraintestinal manifestations (EIMs) occurring in 25-40% of patients. Among these, respiratory complications are of particular concern, yet the immunologic and physiologic mechanisms underlying gut-lung interactions remain poorly understood. The gut-lung axis (GLA) describes bi-directional communication between the gut and lungs, where microbial dysbiosis in the gut can drive lung inflammation and immune dysregulation.

methodsMice were treated with 4% DSS for 7 days to induce colitis. Gut permeability, tight junction protein expression, lung inflammation, immune cell trafficking, and microbial translocation were assessed through histology, qPCR, flow cytometry, and GFP-tagged fecal microbiome experiments.

resultsDSS treatment led to significant disruption of the gut barrier, with upregulation of gut leakage markers and downregulation of tight junction proteins. Lung inflammation was characterized by elevated IL-17, neutrophil infiltration, and airway hyperresponsiveness. Flow cytometry revealed mis-homing of gut-primed immune cells (α4β7+ and CCR9 + CD4+) to the lungs and tracking bacteria via GFP- tagged fecal microbiome confirmed microbial translocation from the gut to the lungs which may contribute to lung inflammation.

conclusionDisrupted gut integrity facilitates microbial translocation and immune cell mis-homing, contributing to lung inflammation. These results provide new insights into how gut dysbiosis influences respiratory inflammation.

Indexed as

DysbiosisGastrointestinal MicrobiomePneumoniaAnimalsColitisDextran SulfateDisease Models, AnimalLungMaleMiceMice, Inbred C57BLDextran Sulfate

Identifiers

PMID40435188
PMCPMC12118880

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.