Evidence map›Paper›PMID 33336693›Full record

ArticleInflammatory bowel diseases2021

Antagonism of Adherent Invasive E. coli LF82 With Human α-defensin 5 in the Follicle-associated Epithelium of Patients With Ileal Crohn's Disease.

Lina Y Alkaissi, Martin E Winberg, Stéphanie D S Heil, Staffan Haapaniemi, Pär Myrelid, Eduard F Stange, Johan D Söderholm, Åsa V Keita

Open access · hybridAbstract read
In one paragraph

Article in Inflammatory bowel diseases, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.6field-weighted citation impact, top 34% 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

3 citing papers in PubMed, 4 citations in OpenAlex.

  1. Role of adherent invasiveWorld journal of clinical cases · 2022
    Review
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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

8 authors at 2 institutions in 2 countries.

Lina Y AlkaissiDepartment of Biomedical and Clinical Sciences, Linköping University, Linköping, Sweden.
Martin E WinbergDepartment of Biomedical and Clinical Sciences, Linköping University, Linköping, Sweden.
Stéphanie D S HeilDepartment of Biomedical and Clinical Sciences, Linköping University, Linköping, Sweden.
Staffan HaapaniemiDepartment of Biomedical and Clinical Sciences, Linköping University, Linköping, Sweden.
Pär MyrelidDepartment of Biomedical and Clinical Sciences, Linköping University, Linköping, Sweden.
Eduard F StangeDepartment of Gastroenterology, Dept. Internal Medicine I, University of Tübingen, 72076 Tübingen, Germany.
Johan D SöderholmDepartment of Biomedical and Clinical Sciences, Linköping University, Linköping, Sweden.
Åsa V KeitaDepartment of Biomedical and Clinical Sciences, Linköping University, Linköping, Sweden.
Linköping University · SEUniversity of Tübingen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe first visible signs of Crohn's disease (CD) are microscopic erosions over the follicle-associated epithelium (FAE). The aim of the study was to investigate the effects of human α-defensin 5 (HD5) on adherent-invasive Escherichia coli LF82 translocation and HD5 secretion after LF82 exposure in an in vitro model of human FAE and in human FAE ex vivo.

methodsAn in vitro FAE-model was set up by the coculture of Raji B cells and Caco-2-cl1 cells. Ileal FAE from patients with CD and controls were mounted in Ussing chambers. The effect of HD5 on LF82 translocation was studied by LF82 exposure to the cells or tissues with or without incubation with HD5. The HD5 secretion was measured in human FAE exposed to LF82 or Salmonella typhimurium. The HD5 levels were evaluated by immunofluorescence, immunoblotting, and ELISA.

resultsThere was an increased LF82 translocation across the FAE-model compared with Caco-2-cl1 (P < 0.05). Incubation of cell/tissues with HD5 before LF82 exposure reduced bacterial passage in both models. Human FAE showed increased LF82 translocation in CD compared with controls and attenuated passage after incubation with sublethal HD5 in both CD and controls (P < 0.05). LF82 exposure resulted in a lower HD5 secretion in CD FAE compared with controls (P < 0.05), whereas Salmonella exposure caused equal secretion on CD and controls. There were significantly lower HD5 levels in CD tissues compared with controls.

conclusionsSublethal HD5 reduces the ability of LF82 to translocate through FAE. The HD5 is secreted less in CD in response to LF82, despite a normal response to Salmonella. This further implicates the integrated role of antimicrobial factors and barrier function in CD pathogenesis.

Indexed as

alpha-DefensinsCrohn DiseaseIleal DiseasesCaco-2 CellsEpitheliumEscherichia coliHumansalpha-Defensinsantimicrobial peptidesbarrier functioninflammatory bowel disease

Identifiers

PMID33336693
PMCPMC8205628
OpenAlexW3115540323

What OpenQuestion holds

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LicenceCC BY-NC
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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.