Evidence map›Paper›PMID 27776487›Full record

ArticleBMC infectious diseases2016

The COX- inhibitor indomethacin reduces Th1 effector and T regulatory cells in vitro in Mycobacterium tuberculosis infection.

Kristian Tonby, Ida Wergeland, Nora V Lieske, Dag Kvale, Kjetil Tasken, Anne M Dyrhol-Riise

Open access · goldAbstract read
In one paragraph

Article in BMC infectious diseases, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

19 citing papers in PubMed, 44 citations in OpenAlex.

  1. Trial
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  4. Article
  5. Article
  6. Host-directed therapy for tuberculosis.European journal of medical research · 2025
    Review
  7. Article
  8. Article
  9. Paradoxical manifestations during tuberculous meningitis treatment among HIV-negative patients: a retrospective descriptive study and literature review.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2022
    Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Prostaglandin EPharmacology & therapeutics · 2018
    Review
  18. Review
  19. 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

6 authors at 3 institutions in 1 country.

Kristian TonbyInstitute of Clinical Medicine, University of Oslo, Oslo, Norway. kristian.tonby@medisin.uio.no.
Ida WergelandDepartment of Clinical Science, University of Bergen, Bergen, Norway.
Nora V LieskeCentre for Molecular Medicine Norway, Nordic EMBL Partnership, University of Oslo, Oslo, Norway.
Dag KvaleInstitute of Clinical Medicine, University of Oslo, Oslo, Norway.
Kjetil TaskenDepartment of Infectious Diseases, Oslo University Hospital, Oslo, Norway.
Anne M Dyrhol-RiiseInstitute of Clinical Medicine, University of Oslo, Oslo, Norway.
University of Oslo · NOOslo University Hospital · NOUniversity of Bergen · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTuberculosis (TB) causes a major burden on global health with long and cumbersome TB treatment regimens. Host-directed immune modulating therapies have been suggested as adjunctive treatment to TB antibiotics. Upregulated cyclooxygenase-2 (COX-2)-prostaglandin E2 (PGE2) signaling pathway may cause a dysfunctional immune response that favors survival and replication of Mycobacterium tuberculosis (Mtb).

methodsBlood samples were obtained from patients with latent TB (n = 9) and active TB (n = 33) before initiation of anti-TB chemotherapy. COX-2 expression in monocytes and ESAT-6 and Ag85 specific T cell cytokine responses (TNF-α, IFN-γ, IL-2), proliferation (carboxyfluorescein succinimidyl ester staining) and regulation (FOXP3+ T regulatory cells) were analysed by flow cytometry and the in vitro effects of the COX-1/2 inhibitor indomethacin were measured.

resultsWe demonstrate that indomethacin significantly down-regulates the fraction of Mtb specific FOXP3+ T regulatory cells (ESAT-6; p = 0.004 and Ag85; p < 0.001) with a concomitant reduction of Mtb specific cytokine responses and T cell proliferation in active TB. Although active TB tend to have higher levels, there are no significant differences in COX-2 expression between unstimulated monocytes from patients with active TB compared to latent infection. Monocytes in both TB groups respond with a significant upregulation of COX-2 after in vitro stimulation.

conclusionsTaken together, our in vitro data indicate a modulation of the Th1 effector and T regulatory cells in Mtb infection in response to the COX-1/2 inhibitor indomethacin. The potential role as adjunctive host-directed therapy in TB disease should be further evaluated in both animal studies and in human clinical trials.

Indexed as

AdolescentAdultAgedAntigens, BacterialCyclooxygenase 2Cyclooxygenase InhibitorsCytokinesFemaleFlow CytometryHumansIndomethacinLatent TuberculosisMaleMiddle AgedMycobacterium tuberculosisTh1 CellsAntigens, BacterialCyclooxygenase 2Cyclooxygenase InhibitorsCytokinesIndomethacinPTGS2 protein, humanTumor Necrosis Factor-alphaCOX-inhibitorsCytokinesHost-directed therapyMonocytesRegulatory T cellsTregsTuberculosis

Identifiers

PMID27776487
PMCPMC5078976
OpenAlexW2535261709

What OpenQuestion holds

Textmetadata
LicenceCC BY
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Registered trials

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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.