Evidence map›Paper›PMID 31517993›Full record

ReviewBritish journal of pharmacology2019

Isoniazid and host immune system interactions: A proposal for a novel comprehensive mode of action.

Saifur R Khan, Yousef Manialawy, Arno G Siraki

Open access · bronzeAbstract readReview
In one paragraph

Review in British journal of pharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 22% 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Preventing Multidrug-Resistant Tuberculosis: The Dawn of a New Era.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2026
    Review
  4. Therapeutic Potential of Isoniazid in Inflammatory Skin Diseases: A Review.Clinical, cosmetic and investigational dermatology · 2026
    Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Observational
  12. Article
  13. Article
  14. Single-Cell Sequencing Reveals Functional Alterations in Tuberculosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
  15. Review
  16. Intracellular Pathogens: Infection, Immunity, and Intervention.Methods in molecular biology (Clifton, N.J.) · 2024
    Review
  17. Review
  18. Horizontal Gene Transfer and Drug Resistance InvolvingAntibiotics (Basel, Switzerland) · 2023
    Article
  19. LncRNA DANCR restrained the survival ofFrontiers in microbiology · 2023
    Article
  20. 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

3 authors at 3 institutions in 1 country.

Saifur R KhanDepartment of Physiology, Faculty of Medicine, University of Toronto, Toronto, Canada.
Yousef ManialawyDepartment of Physiology, Faculty of Medicine, University of Toronto, Toronto, Canada.
Arno G SirakiFaculty of Pharmacy and Pharmaceutical Sciences, University of Alberta, Edmonton, Canada.
Toronto General Hospital · CAUniversity of Alberta · CAUniversity of Toronto · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The known mode of action of isoniazid (INH) is to inhibit bacterial cell wall synthesis following activation by the bacterial catalase-peroxidase enzyme KatG in Mycobacterium tuberculosis (Mtb). This simplistic model fails to explain (a) how isoniazid penetrates waxy granulomas with its very low lipophilicity, (b) how isoniazid kills latent Mtb lacking a typical cell wall, and (c) why isoniazid treatment time is remarkably long in contrast to most other antibiotics. To address these questions, a novel comprehensive mode of action of isoniazid has been proposed here. Briefly, isoniazid eradicates latent tuberculosis (TB) by prompting slow differentiation of pro-inflammatory monocytes and providing protection against reactive species-induced "self-necrosis" of phagocytes. In the case of active TB, different immune cells form INH-NAD

Indexed as

Antitubercular AgentsBacterial ProteinsCatalaseHost Microbial InteractionsHumansIsoniazidMonocytesMycobacterium tuberculosisOxidative StressTuberculosisAntitubercular AgentsBacterial ProteinsCatalaseIsoniazidkatG protein, Mycobacterium tuberculosis

Identifiers

PMID31517993
PMCPMC6965675
OpenAlexW2972910926

What OpenQuestion holds

Textmetadata
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.