Evidence map›Paper›PMID 29228057›Full record

ArticlePloS one2017

N-acetylcysteine (NAC) ameliorates Epstein-Barr virus latent membrane protein 1 induced chronic inflammation.

Xiao Gao, Eirini-Maria Lampraki, Sarwah Al-Khalidi, Muhammad Asif Qureshi, Rhea Desai, Joanna Beatrice Wilson

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. 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
0.4field-weighted citation impact, top 35% 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, 16 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
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  11. N-acetylcysteine and coronavirus disease 2019: May it work as a beneficial preventive and adjuvant therapy? A comprehensive review study.Journal of research in medical sciences : the official journal of Isfahan University of Medical Sciences · 2020
    Review
  12. BioMed research international · 2019
    Article
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

6 authors at 1 institution in 1 country.

Xiao GaoCollege of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, United Kingdom.
Eirini-Maria LamprakiCollege of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, United Kingdom.ORCID http://orcid.org/0000-0002-5688-8542
Sarwah Al-KhalidiCollege of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, United Kingdom.
Muhammad Asif QureshiCollege of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, United Kingdom.
Rhea DesaiCollege of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, United Kingdom.
Joanna Beatrice WilsonCollege of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, United Kingdom.ORCID http://orcid.org/0000-0003-4715-2530
University of Glasgow · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic inflammation results when the immune system responds to trauma, injury or infection and the response is not resolved. It can lead to tissue damage and dysfunction and in some cases predispose to cancer. Some viruses (including Epstein-Barr virus (EBV)) can induce inflammation, which may persist even after the infection has been controlled or cleared. The damage caused by inflammation, can itself act to perpetuate the inflammatory response. The latent membrane protein 1 (LMP1) of EBV is a pro-inflammatory factor and in the skin of transgenic mice causes a phenotype of hyperplasia with chronic inflammation of increasing severity, which can progress to pre-malignant and malignant lesions. LMP1 signalling leads to persistent deregulated expression of multiple proteins throughout the mouse life span, including TGFα S100A9 and chitinase-like proteins. Additionally, as the inflammation increases, numerous chemokines and cytokines are produced which promulgate the inflammation. Deposition of IgM, IgG, IgA and IgE and complement activation form part of this process and through genetic deletion of CD40, we show that this contributes to the more tissue-destructive aspects of the phenotype. Treatment of the mice with N-acetylcysteine (NAC), an antioxidant which feeds into the body's natural redox regulatory system through glutathione synthesis, resulted in a significantly reduced leukocyte infiltrate in the inflamed tissue, amelioration of the pathological features and delay in the inflammatory signature measured by in vivo imaging. Reducing the degree of inflammation achieved through NAC treatment, had the knock on effect of reducing leukocyte recruitment to the inflamed site, thereby slowing the progression of the pathology. These data support the idea that NAC could be considered as a treatment to alleviate chronic inflammatory pathologies, including post-viral disease. Additionally, the model described can be used to effectively monitor and accurately measure therapies for chronic inflammation.

Indexed as

AcetylcysteineAnimalsChronic DiseaseHerpesvirus 4, HumanInflammationMiceMice, TransgenicViral Matrix ProteinsAcetylcysteineEBV-associated membrane antigen, Epstein-Barr virusViral Matrix Proteins

Identifiers

PMID29228057
PMCPMC5724866
OpenAlexW2774436577

What OpenQuestion holds

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LicenceCC BY
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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.