Evidence map›Paper›PMID 30884758›Full record

ArticleCells2019

Lack of Small Intestinal Dysbiosis Following Long-Term Selective Inhibition of Cyclooxygenase-2 by Rofecoxib in the Rat.

Bernadette Lázár, Gábor B Brenner, András Makkos, Mihály Balogh, Szilvia B László, Mahmoud Al-Khrasani, Barbara Hutka, Emese Bató, Eszter Ostorházi, János Juhász and 10 more

Open access · goldAbstract read
In one paragraph

Article in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

5 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. NSAID-Gut Microbiota Interactions.Frontiers in pharmacology · 2020
    Review
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

20 authors at 4 institutions in 1 country.

Bernadette LázárDepartment of Pharmacology and Pharmacotherapy, Semmelweis University, 1089 Budapest, Hungary. lazar.bernadette@med.semmelweis-univ.hu.
Gábor B BrennerDepartment of Pharmacology and Pharmacotherapy, Semmelweis University, 1089 Budapest, Hungary. brenner.gabor@med.semmelweis-univ.hu.
András MakkosDepartment of Pharmacology and Pharmacotherapy, Semmelweis University, 1089 Budapest, Hungary. makkos.andras@med.semmelweis-univ.hu.
Mihály BaloghDepartment of Pharmacology and Pharmacotherapy, Semmelweis University, 1089 Budapest, Hungary. balogh.mihaly@med.semmelweis-univ.hu.ORCID 0000-0003-3296-0316
Szilvia B LászlóDepartment of Pharmacology and Pharmacotherapy, Semmelweis University, 1089 Budapest, Hungary. laszlo.szilvia@med.semmelweis-univ.hu.
Mahmoud Al-KhrasaniDepartment of Pharmacology and Pharmacotherapy, Semmelweis University, 1089 Budapest, Hungary. al-khrasani.mahmoud@med.semmelweis-univ.hu.
Barbara HutkaDepartment of Pharmacology and Pharmacotherapy, Semmelweis University, 1089 Budapest, Hungary. hutka.barbara@gmail.com.
Emese BatóSecond Department of Internal Medicine and Cardiology Center, University of Szeged, 6725 Szeged, Hungary. horeyezonr@gmail.com.
Eszter OstorháziInstitute of Medical Microbiology, Semmelweis University, 1089 Budapest, Hungary. droeszter@gmail.com.
János JuhászFaculty of Information Technology and Bionics, Pázmány Péter Catholic University, 1083 Budapest, Hungary. juhaszjanos4@gmail.com.ORCID 0000-0002-1307-7387
Ágnes KeményDepartment of Medical Biology, University of Pécs, 7624 Pécs, Hungary. kemenyagnes1@gmail.com.ORCID 0000-0002-4523-3938
Terézia LászlóDepartment of Pathology, University of Pécs, 7624 Pécs, Hungary. laszlo.terezia@med.semmelweis-univ.hu.
László TiszlaviczDepartment of Pathology, University of Szeged, 6725 Szeged, Hungary. tiszlavicz.laszlo@med.u-szeged.hu.
Zoltán BihariXenovea Ltd., 6726 Szeged, Hungary. info.xenovea@gmail.com.
Zoltán GiriczDepartment of Pharmacology and Pharmacotherapy, Semmelweis University, 1089 Budapest, Hungary. giricz.zoltan@med.semmelweis-univ.hu.
Dóra SzabóInstitute of Medical Microbiology, Semmelweis University, 1089 Budapest, Hungary. szabo.dora@med.semmelweis-univ.hu.
Zsuzsanna HelyesDepartment of Pharmacology and Pharmacotherapy, Medical School & Szentágothai Research Centre, University of Pécs, 7624 Pécs, Hungary. zsuzsanna.helyes@aok.pte.hu.
Péter FerdinandyDepartment of Pharmacology and Pharmacotherapy, Semmelweis University, 1089 Budapest, Hungary. peter.ferdinandy@pharmahungary.com.
Klára GyiresDepartment of Pharmacology and Pharmacotherapy, Semmelweis University, 1089 Budapest, Hungary. gyires.klara@med.semmelweis-univ.hu.
Zoltán S ZádoriDepartment of Pharmacology and Pharmacotherapy, Semmelweis University, 1089 Budapest, Hungary. zadori.zoltan@med.semmelweis-univ.hu.ORCID 0000-0001-7312-618X
Semmelweis University · HUUniversity of Pecs · HUUniversity of Szeged · HUPázmány Péter Catholic University · HU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Intestinal dysbiosis is linked to numerous gastrointestinal disorders, including inflammatory bowel diseases. It is a question of debate if coxibs, selective inhibitors of cyclooxygenase (COX)-2, cause dysbiosis. Therefore, in the present study, we aimed to determine the effect of long-term (four weeks) selective inhibition of COX-2 on the small intestinal microbiota in the rat. In order to avoid mucosal damage due to topical effects and inflammation-driven microbial alterations, rofecoxib, a nonacidic compound, was used. The direct inhibitory effect of rofecoxib on the growth of bacteria was ruled out in vitro. The mucosa-sparing effect of rofecoxib was confirmed by macroscopic and histological analysis, as well as by measuring the intestinal levels of cytokines and tight junction proteins. Deep sequencing of bacterial 16S rRNA revealed that chronic rofecoxib treatment had no significant influence on the composition and diversity of jejunal microbiota. In conclusion, this is the first demonstration that long-term selective inhibition of COX-2 by rofecoxib does not cause small intestinal dysbiosis in rats. Moreover, inhibition of COX-2 activity is not likely to be responsible per se for microbial alterations caused by some coxibs, but other drug-specific properties may contribute to it.

Indexed as

AnimalsBacteriaCelecoxibCyclooxygenase 2Cyclooxygenase 2 InhibitorsDinoprostoneDysbiosisGastric MucosaGastrointestinal MicrobiomeIntestine, SmallLactonesMaleMicrobial Sensitivity TestsRats, WistarSulfonesTime FactorsCelecoxibCyclooxygenase 2Cyclooxygenase 2 InhibitorsDinoprostoneLactonesrofecoxibSulfonescyclooxygenase-2enteropathyinflammatory bowel diseasesintestinal dysbiosismicrobiotarofecoxib

Identifiers

PMID30884758
PMCPMC6468807
OpenAlexW2921181004

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.