Evidence map›Paper›PMID 22992722›Full record

ArticleGenes and immunity2012

Host gene-encoded severe lung TB: from genes to the potential pathways.

M Ganachari, H Guio, N Zhao, P O Flores-Villanueva

Open access · bronzeAbstract read
In one paragraph

Article in Genes and immunity, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 23% 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

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

  1. Pooled it
  2. Article
  3. Article
  4. Single nucleotide variants in theFrontiers in cellular and infection microbiology · 2024
    Observational
  5. Article
  6. Genetics and evolution of tuberculosis pathogenesis: New perspectives and approaches.Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases · 2020
    Review
  7. Article
  8. Review
  9. Genetics and genomics in Peru: Clinical and research perspective.Molecular genetics & genomic medicine · 2018
    Review
  10. Tuberculosis and lung damage: from epidemiology to pathophysiology.European respiratory review : an official journal of the European Respiratory Society · 2018
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. 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 4 institutions in 2 countries.

M GanachariCenter for Molecular and Translational Human Infectious Diseases Research, The Methodist Hospital Research Institute, Houston, TX 77030, USA.
H Guio
N Zhao
P O Flores-Villanueva
Cornell University · USHouston Methodist · USMethodist Hospital · USNational Institute of Quality · PE

Funding

MCP-1 and MMP-1 contributions in susceptibility to developing active tuberculosisR01HL084347 · NHLBI · UNIVERSITY OF TEXAS HLTH CTR AT TYLER · PI FLORES-VILLANUEVA, PEDRO OMAR · 2006 to 2010
$1.7M
NHLBI NIH HHS R01 HL084347NHLBI NIH HHS R01 HL084347-06
6 · The paper itself

Abstract

We are reporting that the two-locus genotype -2518 macrophage chemoattractant protein (MCP)-1 GG and -1607 matrix metalloproteinase (MMP)-1 2G/2G promotes the expression of hyperinflammation in response to Mycobacterium tuberculosis infection, inducing extensive tissue damage and severe tuberculosis (TB) disease. Carriers of this two-locus genotype have a 13-fold higher chance of developing severe disease and 6.5-fold higher chance of developing permanent lesions, and a 3.864-fold higher chance of delayed response to first-line standardized treatment than carriers of any other relevant combination of genotypes at those two loci. Thus, these persons have an increased likelihood of poor health-related quality of life and of transmitting M. tuberculosis to other members of the community. In addition, through the analysis of human lung tissues, serum/plasma and in vitro experiments, including in vitro infections of THP-1 cells with M. tuberculosis and microarray analysis, we determined that this hyperinflammation state is potentially driven by the MCP-1/MMP-1/PAR-1 pathway. Hence, we are providing markers for the identification of TB cases that may develop severe pulmonary disease and delayed response to treatment, and are providing the basis for development of novel host-targeted clinical interventions to ameliorate the severity of pulmonary TB.

Indexed as

Genetic LociGenetic Predisposition to DiseasePolymorphism, Single NucleotideAdultAntitubercular AgentsBiomarkersCell LineChemokine CCL2Drug Resistance, Multiple, BacterialFemaleGene Expression RegulationHost-Pathogen InteractionsHumansInflammationMaleMatrix Metalloproteinase 1Antitubercular AgentsBiomarkersCCL2 protein, humanChemokine CCL2Matrix Metalloproteinase 1Receptor, PAR-1

Identifiers

PMID22992722
PMCPMC3518758
OpenAlexW2094379184

What OpenQuestion holds

Textmetadata
LicenceTDM
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.