Evidence map›Paper›PMID 25269707›Full record

ArticleMucosal immunology2015

Subversion of human intestinal mucosa innate immunity by a Crohn's disease-associated E. coli.

A Jarry, L Crémet, N Caroff, C Bou-Hanna, J M Mussini, A Reynaud, A L Servin, J F Mosnier, V Liévin-Le Moal, C L Laboisse

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Mucosal immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.9field-weighted citation impact, top 17% 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

12 citing papers in PubMed, 20 citations in OpenAlex.

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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

10 authors at 3 institutions in 1 country.

A JarryEA 4273 Biometadys, Université de Nantes, Faculté de Médecine, Nantes, France.
L Crémet1] UPRES EA3826 Université de Nantes, Faculté de Médecine, Nantes, France [2] CHU Nantes, Service de Bactériologie-Hygiène, Nantes, France.
N Caroff1] UPRES EA3826 Université de Nantes, Faculté de Médecine, Nantes, France [2] CHU Nantes, Service de Bactériologie-Hygiène, Nantes, France.
C Bou-HannaEA 4273 Biometadys, Université de Nantes, Faculté de Médecine, Nantes, France.
J M MussiniCHU Nantes, Service d'Anatomie et Cytologie Pathologiques, Nantes, France.
A Reynaud1] UPRES EA3826 Université de Nantes, Faculté de Médecine, Nantes, France [2] CHU Nantes, Service de Bactériologie-Hygiène, Nantes, France.
A L ServinCNRS UMR8076, Université Paris-Sud, Faculté de Pharmacie, Chatenay-Malabry, France.
J F Mosnier1] EA 4273 Biometadys, Université de Nantes, Faculté de Médecine, Nantes, France [2] CHU Nantes, Service d'Anatomie et Cytologie Pathologiques, Nantes, France.
V Liévin-Le MoalCNRS UMR8076, Université Paris-Sud, Faculté de Pharmacie, Chatenay-Malabry, France.
C L Laboisse1] EA 4273 Biometadys, Université de Nantes, Faculté de Médecine, Nantes, France [2] CHU Nantes, Service d'Anatomie et Cytologie Pathologiques, Nantes, France.
Centre Hospitalier Universitaire de Nantes · FRNantes Université · FRUniversité Paris-Sud · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Adherent-invasive Escherichia coli (AIEC), associated with Crohn's disease, are likely candidate contributory factors in the disease. However, signaling pathways involved in human intestinal mucosa innate host response to AIEC remain unknown. Here we use a 3D model of human intestinal mucosa explant culture to explore the effects of the AIEC strain LF82 on two innate immunity platforms, i.e., the inflammasome through evaluation of caspase-1 status, and NFκB signaling. We showed that LF82 bacteria enter and survive within a few intestinal epithelial cells and macrophages, without altering the mucosa overall architecture. Although 4-h infection with a Salmonella strain caused crypt disorganization, caspase-1 activation, and mature IL-18 production, LF82 bacteria were unable to activate caspase-1 and induce IL-18 production. In parallel, LF82 bacteria activated NFκB signaling in epithelial cells through IκBα phosphorylation, NFκBp65 nuclear translocation, and TNFα secretion. In addition, NFκB activation was crucial for the maintenance of epithelial homeostasis upon LF82 infection. In conclusion, here we decipher at the whole-mucosa level the mechanisms of the LF82-induced subversion of innate immunity that, by maintaining host cell integrity, ensure intracellular bacteria survival.

Indexed as

Immune EvasionImmunity, InnateCaspase 1Crohn DiseaseEpithelial CellsGene Expression RegulationHumansI-kappa B ProteinsImmunity, MucosalInflammasomesInterleukin-18Intestinal MucosaMacrophagesNF-KappaB Inhibitor alphaPhosphorylationSalmonellaCaspase 1I-kappa B ProteinsIL18 protein, humanInflammasomesInterleukin-18NF-KappaB Inhibitor alphaNFKBIA protein, humanTranscription Factor RelATumor Necrosis Factor-alpha

Identifiers

PMID25269707
OpenAlexW1989327683

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.