Evidence map›Paper›PMID 26722451›Full record

ArticleInternational journal of clinical and experimental pathology2015

Genetic polymorphisms of CCL1 rs2072069 G/A and TLR2 rs3804099 T/C in pulmonary or meningeal tuberculosis patients.

Yue Zhao, Hui Bu, Kun Hong, Hua Yin, Yue-Li Zou, Shu-Jun Geng, Ming-Ming Zheng, Jun-Ying He

Open access · greenAbstract read
In one paragraph

Article in International journal of clinical and experimental pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
3.8field-weighted citation impact, top 7% 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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.

  1. Pooled it
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  7. Offense and Defense in Granulomatous Inflammation Disease.Frontiers in cellular and infection microbiology · 2022
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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

8 authors at 2 institutions in 1 country.

Yue ZhaoDepartment of Neurology, The Second Hospital of Hebei Medical University Shijiazhuang, Hebei, China.
Hui BuDepartment of Neurology, The Second Hospital of Hebei Medical University Shijiazhuang, Hebei, China.
Kun HongDepartment of Neurology, The Second Hospital of Hebei Medical University Shijiazhuang, Hebei, China.
Hua YinDepartment of Neurology, The Second Hospital of Hebei Medical University Shijiazhuang, Hebei, China.
Yue-Li ZouDepartment of Neurological Laboratory of Hebei Province, The Second Hospital of Hebei Medical University Shijiazhuang, Hebei, China.
Shu-Jun GengDepartment of Internal Medicine-Tuberculosis, The Hebei Provincial Chest Hospital Shijiazhuang, Hebei, China.
Ming-Ming ZhengDepartment of Neurology, The Second Hospital of Hebei Medical University Shijiazhuang, Hebei, China.
Jun-Ying HeDepartment of Neurology, The Second Hospital of Hebei Medical University Shijiazhuang, Hebei, China.
Hebei Medical University · CNHospital of Hebei Province · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CCL1, one of the members of the CC chemokine family, is an inflammatory mediator that stimulates the migration of human monocytes. CCL1 expression is induced by Mycobacterium tuberculosis and TLR ligands in macrophage. TLR2 plays critical role in host immune response against M. tuberculosis infection by regulating the macrophage activation and cytokine secretion. M. tuberculosis causes different clinical forms of tuberculosis (TB) disease. Single-nucleotide polymorphisms (SNPs) in the CCL1 gene and TLR2 gene may be associated with the development of different clinical forms of TB, depending on the different immune mechanisms. This study was to evaluate the possible association between CCL1 rs2072069 G/A or/and TLR2 rs3804099 T/C (T597C) polymorphisms and pulmonary tuberculosis (PTB) or/and tuberculous meningitis (TBM) in a sample of the Chinese adult population. A case-control study was designed to compare the allele frequency and genotype distribution between control (n=386) and TB (n=341) who had either PTB (n=230) or TBM (n=111). The genotype typing was performed using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) technique. TLR2 variant genotype 597CC was associated with susceptibility to PTB rather than to TBM. In the male PTB subgroup, 597CC genotype was identified in a higher rate, compared with male control subgroup. This study demonstrates that T597C polymorphism of TLR2 is a risk factor for susceptibility to PTB rather than to TBM in a sample of Chinese adult population. Patient gender may affect the outcome of M. tuberculosis infection. TLR2 gene may influence the development of PTB and TBM by different immune mechanisms.

Indexed as

Polymorphism, Single NucleotideAdultAsian PeopleCase-Control StudiesChemokine CCL1FemaleGenetic Predisposition to DiseaseGenotypeHumansMaleMiddle AgedPolymerase Chain ReactionPolymorphism, Restriction Fragment LengthToll-Like Receptor 2Tuberculosis, MeningealTuberculosis, PulmonaryCCL1 protein, humanChemokine CCL1TLR2 protein, humanToll-Like Receptor 2CCL1polymorphismpulmonary tuberculosis (PTB)TLR2tuberculosis (TB)tuberculous meningitis (TBM)

Identifiers

PMID26722451
PMCPMC4680396
OpenAlexW2197231704

What OpenQuestion holds

Textmetadata
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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.