Evidence map›Paper›PMID 31203717›Full record

ArticleGut microbes2020

Lipopolysaccharides modulate intestinal epithelial permeability and inflammation in a species-specific manner.

Matthew Stephens, Pierre-Yves von der Weid

Open access · goldAbstract read
In one paragraph

Article in Gut microbes, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 170 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
170citing papers in PubMed, 1 pooled it
10.2field-weighted citation impact, top 1% of its field
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

170 citing papers in PubMed, 1 synthesis or guideline pooled it, 272 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Gut microbiota: contributing to high CVD prevalence in people living with schizophrenia?European archives of psychiatry and clinical neuroscience · 2026
    Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Review
  17. RNF168 promotes chronic colitis through ANXA7-mediated autophagy and NLRP3-driven pyroptosis.Apoptosis : an international journal on programmed cell death · 2026
    Article
  18. Article
  19. Article
  20. Article

110 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Matthew StephensSnyder Institute for Chronic Diseases, Department of Physiology & Pharmacology, Cumming School of Medicine, University of Calgary , Calgary, Canada.
Pierre-Yves von der WeidSnyder Institute for Chronic Diseases, Department of Physiology & Pharmacology, Cumming School of Medicine, University of Calgary , Calgary, Canada.
University of Calgary · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Patients presenting with Inflammatory bowel disease have been shown to exhibit an altered microbiome in both Crohn's disease and Ulcerative colitis. This shift in the microbial content led us to question whether several of these microbes are important in inflammatory processes present in these diseases and more specifically whether lipopolysaccharides from the gram-negative cell wall differentially stimulates resident cells. We, therefore, investigated the possible contribution of five major species of gram-negative bacteria found to be altered in presence during disease progression and evaluate their pathogenicity through LPS. We demonstrated that LPS from these different species had individual capacities to induce NF-κB and pro-inflammatory IL-8 production from HEK-TLR4 cells in a TLR4 dependent manner. Additional work using human intestinal colonic epithelial cell monolayers (Caco-2) demonstrated that the cells responded to the serotype specific LPS in a distinct manner, inducing many inflammatory mediators such as TNF-α and IL-10 in significantly altered proportions. Furthermore, the permeability of Caco-2 monolayers, as a test for their ability to alter intestinal permeability, was also differentially altered by the serotype specific LPS modulating trans-epithelial electrical resistance, small molecule movement, and tight junction integrity. Our results suggest that specific species of bacteria may be potentiating the pathogenesis of IBD and chronic inflammatory diseases through their serotype specific LPS responses.

Indexed as

Caco-2 CellsCell LineCell SurvivalCytokinesEpithelial CellsGram-Negative BacteriaHumansInflammationInflammatory Bowel DiseasesInterleukin-8IntestinesLipopolysaccharidesNF-kappa BPermeabilitySpecies SpecificityTight JunctionsCXCL8 protein, humanCytokinesInterleukin-8LipopolysaccharidesNF-kappa BTLR4 protein, humanToll-Like Receptor 4EndotoxinEpitheliumInflammationLipopolysaccharidesToll- like receptor 4

Identifiers

PMID31203717
PMCPMC7524286
OpenAlexW2951541824

What OpenQuestion holds

Textmetadata
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.