Evidence map›Paper›PMID 24766519›Full record

ArticleImmunology2014

Mycobacterium indicus pranii and Mycobacterium bovis BCG lead to differential macrophage activation in Toll-like receptor-dependent manner.

Pawan Kumar, Rohit Tyagi, Gobardhan Das, Sangeeta Bhaskar

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

30 citing papers in PubMed, 45 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Frontiers in immunology · 2024
    Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Observational
  10. Cytokine Storm and Immunomodulation in COVID-19.Indian journal of critical care medicine : peer-reviewed, official publication of Indian Society of Critical Care Medicine · 2021
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Journal of immunology research · 2019
    Article
  19. 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

4 authors at 2 institutions in 1 country.

Pawan KumarNational Institute of Immunology, New Delhi, India.
Rohit Tyagi
Gobardhan Das
Sangeeta Bhaskar
National Institute of Immunology · INInternational Centre for Genetic Engineering and Biotechnology · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mycobacterium indicus pranii (MIP) is an atypical mycobacterial species possessing strong immunomodulatory properties. It is a potent vaccine candidate against tuberculosis, promotes Th1 immune response and protects mice from tumours. In previous studies, we demonstrated higher protective efficacy of MIP against experimental tuberculosis as compared with bacillus Calmette-Guérin (BCG). Since macrophages play an important role in the pathology of mycobacterial diseases and cancer, in the present study, we evaluated the MIP in live and killed form for macrophage activation potential, compared it with BCG and investigated the underlying mechanisms. High levels of tumour necrosis factor-α, interleukin-12p40 (IL-12p40), IL-6 and nitric oxide were produced by MIP-stimulated macrophages as compared with BCG-stimulated macrophages. Prominent up-regulation of co-stimulatory molecules CD40, CD80 and CD86 was also observed in response to MIP. Loss of response in MyD88-deficient macrophages showed that both MIP and BCG activate the macrophages in a MyD88-dependent manner. MyD88 signalling pathway culminates in nuclear factor-κB/activator protein-1 (NF-κB/AP-1) activation and higher activation of NF-κB/AP-1 was observed in response to MIP. With the help of pharmacological inhibitors and Toll-like receptor (TLR) -deficient macrophages, we observed the role of TLR2, TLR4 and intracellular TLRs in MIP-mediated macrophage activation. Stimulation of HEK293 cells expressing TLR2 in homodimeric or heterodimeric form showed that MIP has a distinctly higher level of TLR2 agonist activity compared with BCG. Further experiments suggested that TLR2 ligands are well exposed in MIP whereas they are obscured in BCG. Our findings establish the higher macrophage activation potential of MIP compared with BCG and delineate the underlying mechanism.

Indexed as

Macrophage ActivationAnimalsHEK293 CellsHumansInflammation MediatorsInterleukin-10Interleukin-12 Subunit p40Interleukin-6Macrophages, PeritonealMiceMice, Inbred C57BLMice, KnockoutMycobacterium bovisMyeloid Differentiation Factor 88NF-kappa BNitric OxideIL10 protein, mouseInflammation MediatorsInterleukin-10Interleukin-12 Subunit p40Interleukin-6interleukin-6, mouseMyd88 protein, mouseMyeloid Differentiation Factor 88NF-kappa BNitric OxideTlr2 protein, mouseTlr4 protein, mouseToll-Like Receptor 2Toll-Like Receptor 4Transcription Factor AP-1Tumor Necrosis Factor-alphabacterialcytokinesToll-like receptors

Identifiers

PMID24766519
PMCPMC4172141
OpenAlexW2071899866

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.