Evidence map›Paper›PMID 34210024›Full record

ArticleViruses2021

Epstein-Barr Virus DNA Exacerbates Colitis Symptoms in a Mouse Model of Inflammatory Bowel Disease.

Sirine Andari, Hadi Hussein, Sukayna Fadlallah, Abdo R Jurjus, Margret Shirinian, Jana G Hashash, Elias A Rahal

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Viruses, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.1field-weighted citation impact, top 20% 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

10 citing papers in PubMed, 17 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

7 authors at 2 institutions in 1 country.

Sirine AndariDepartment of Experimental Pathology, Immunology and Microbiology, American University of Beirut, Beirut, Lebanon.
Hadi HusseinDepartment of Experimental Pathology, Immunology and Microbiology, American University of Beirut, Beirut, Lebanon.
Sukayna FadlallahDepartment of Experimental Pathology, Immunology and Microbiology, American University of Beirut, Beirut, Lebanon.
Abdo R JurjusDepartment of Anatomy, Cell Biology and Physiological Sciences, Faculty of Medicine, American University of Beirut, Beirut, Lebanon.
Margret ShirinianDepartment of Experimental Pathology, Immunology and Microbiology, American University of Beirut, Beirut, Lebanon.
Jana G HashashDivision of Gastroenterology, American University of Beirut Medical Center, Beirut, Lebanon.
Elias A RahalDepartment of Experimental Pathology, Immunology and Microbiology, American University of Beirut, Beirut, Lebanon.ORCID 0000-0002-1096-7042
American University of Beirut · LBAmerican University of Beirut Medical Center · LB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Infection with EBV has been associated with various inflammatory disorders including inflammatory bowel diseases (IBD). Contribution of this virus to intestinal disease processes has not been assessed. We previously detected that EBV DNA triggers proinflammatory responses via the activation of endosomal Toll-like receptor (TLR) signaling. Hence, to examine the colitogenic potential of EBV DNA, we used the dextran sodium sulfate (DSS) mouse colitis model. C57BL/6J mice received either DSS-containing or regular drinking water. Mice were then administered EBV DNA by rectal gavage. Administration of EBV DNA to the DSS-fed mice aggravated colonic disease activity as well as increased the damage to the colon histologic architecture. Moreover, we observed enhanced expression of IL-17A, IFNγ and TNFα in colon tissues from the colitis mice (DSS-treated) given the EBV DNA compared to the other groups. This group also had a marked decrease in expression of the CTLA4 immunoregulatory marker. On the other hand, we observed enhanced expression of endosomal TLRs in colon tissues from the EBV DNA-treated colitis mice. These findings indicate that EBV DNA exacerbates proinflammatory responses in colitis. The ubiquity of EBV in the population indicates that possible similar responses may be of pertinence in a relevant proportion of IBD patients.

Indexed as

AnimalsColonDisease Models, AnimalDisease ProgressionDNA, ViralEpstein-Barr Virus InfectionsFemaleHerpesvirus 4, HumanInflammatory Bowel DiseasesIntestinal MucosaMiceMice, Inbred C57BLSignal TransductionToll-Like ReceptorsDNA, ViralToll-Like ReceptorsEpstein–Barr virusIL-17Ainflammatory bowel diseaseToll-like Receptors

Identifiers

PMID34210024
PMCPMC8310145
OpenAlexW3177075541

What OpenQuestion holds

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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.