Evidence map›Paper›PMID 34307194›Full record

Trial reportFrontiers in cellular and infection microbiology2021

Plasma LOX-Products and Monocyte Signaling Is Reduced by Adjunctive Cyclooxygenase-2 Inhibitor in a Phase I Clinical Trial of Tuberculosis Patients.

Marthe Jøntvedt Jørgensen, Kristin G Nore, Hans Christian D Aass, Emilie Layre, Jérôme Nigou, Rasmus Mortensen, Kjetil Tasken, Dag Kvale, Synne Jenum, Kristian Tonby and 1 more

Open access · goldAbstract readClinical Trial, Phase IRandomized Controlled Trial
In one paragraph

Trial report in Frontiers in cellular and infection microbiology, 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
0.3field-weighted citation impact, top 39% 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, 6 citations in OpenAlex.

  1. Trial
  2. Trial
  3. 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

11 authors at 5 institutions in 3 countries.

Marthe Jøntvedt JørgensenInstitute of Clinical Medicine, University of Oslo, Oslo, Norway.
Kristin G NoreInstitute of Clinical Medicine, University of Oslo, Oslo, Norway.
Hans Christian D AassDepartment of Medical Biochemistry, Oslo University Hospital, Oslo, Norway.
Emilie LayreInstitut de Pharmacologie et de Biologie Structurale, Université de Toulouse, CNRS, Université Paul Sabatier, Toulouse, France.
Jérôme NigouInstitut de Pharmacologie et de Biologie Structurale, Université de Toulouse, CNRS, Université Paul Sabatier, Toulouse, France.
Rasmus MortensenDepartment of Infectious Disease Immunology, Statens Serum Institut, Copenhagen, Denmark.
Kjetil TaskenInstitute of Clinical Medicine, University of Oslo, Oslo, Norway.
Dag KvaleInstitute of Clinical Medicine, University of Oslo, Oslo, Norway.
Synne JenumDepartment of Infectious Diseases, Oslo University Hospital, Oslo, Norway.
Kristian TonbyInstitute of Clinical Medicine, University of Oslo, Oslo, Norway.
Anne Ma Dyrhol-RiiseInstitute of Clinical Medicine, University of Oslo, Oslo, Norway.
University of Oslo · NOOslo University Hospital · NOCentre National de la Recherche Scientifique · FRStatens Serum Institut · DKUniversité Fédérale de Toulouse Midi-Pyrénées · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Eicosanoids and intracellular signaling pathways are potential targets for host-directed therapy (HDT) in tuberculosis (TB). We have explored the effect of cyclooxygenase 2 inhibitor (COX-2i) treatment on eicosanoid levels and signaling pathways in monocytes. Methods: Peripheral blood mononuclear cells isolated from TB patients included in a randomized phase I clinical trial of standard TB treatment with (n=21) or without (n=18) adjunctive COX-2i (etoricoxib) were analyzed at baseline, day 14 and day 56. Plasma eicosanoids were analyzed by ELISA and liquid chromatography-mass spectrometry (LC-MS), plasma cytokines by multiplex, and monocyte signaling by phospho-flow with a defined set of phospho-specific antibodies. Results: Lipoxygenase (LOX)-derived products (LXA4 and 12-HETE) and pro-inflammatory cytokines were associated with TB disease severity and were reduced during TB therapy, possibly accelerated by adjunctive COX-2i. Phosphorylation of p38 MAPK, NFkB, Erk1/2, and Akt in monocytes as well as plasma levels of MIG/CXCL9 and procalcitonin were reduced in the COX-2i group compared to controls. Conclusion: COX-2i may reduce excess inflammation in TB

Indexed as

Cyclooxygenase 2 InhibitorsTuberculosisEicosanoidsHumansLeukocytes, MononuclearLipoxygenaseMonocytesCyclooxygenase 2 InhibitorsEicosanoidsLipoxygenasecyclooxygenase-2 inhibitorcytokineseicosanoidshost-directed therapy (HDT)innate immunitylipooxygenasemonocytestuberculosis

Identifiers

PMID34307194
PMCPMC8299478
OpenAlexW3182947028

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.