Vitamin D receptor FokI gene polymorphism and tuberculosis susceptibility: a meta-analysis

Sun, Ya‐Ping; Cai, Qingshan

doi:10.4238/2015.june.9.1

Cited by 14 publications

(7 citation statements)

References 34 publications

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“…Moderate heterogeneity was found in this study. However, heterogeneity was significantly reduced compared with previous meta-analyses [ 20 , 21 ]. These results not only could confirm HIV infection status as the main source of heterogeneity in previous meta-analyses, but are also the reason why we conducted this study.…”

Section: Discussionmentioning

confidence: 62%

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Vitamin D Receptor Gene FOKI Polymorphism Contributes to Increasing the Risk of HIV-Negative Tuberculosis: Evidence from a Meta-Analysis

Tang

Ding

et al. 2015

PLoS ONE

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BackgroundVitamin D receptor (VDR) gene FokI polymorphism have been studied in relation to tuberculosis (TB) in many populations and provided inconsistent results. In this study, we carried out a meta-analysis to derive a more reliable assessment on FokI polymorphism and the risk of HIV-negative TB.MethodsThe Embase, PubMed, and Cochrane Library databases were used to undertake a comprehensive systematic literature review of all current published VDR gene FOKI association studies aimed at the risk of TB up to June 30, 2015. Odds ratios (ORs) and the corresponding 95% confidence intervals (CIs) were used to measure the strength of the models.ResultsA total of 14 studies (1,668 cases and 1,893 controls) were retrieved in the meta-analysis. The pooled OR was 1.60 (95% = 1.28–1.97, P<0.001; I 2 = 29.5%, and P = 0.141 for heterogeneity) in the best genetic model (recessive model: ff vs. fF+FF). In the subgroup analysis by ethnicities, a significantly increased risk was found in the Asian group (OR = 1.82, 95% CI = 1.42–2.33, P<0.001; I 2 = 31.0%, and P = 0.150 for heterogeneity) in the recessive model. Similarly, significant associations were also found in the polymerase chain reaction-restriction fragment length polymorphism group, high-quality studies, and the population based or hospital based groups. Moderate heterogeneity was found in this study.ConclusionOur results suggested that VDR FokI polymorphism contributes to increasing the risk of TB in HIV-negative individuals, especially in the Asian region. Further studies on this topic in other races are expected to be conducted in future.

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Section: Discussionmentioning

confidence: 62%

“…However, previous literature about the associations between Fok I polymorphism and the risk of TB has provided inconsistent results [ 6 – 19 ]. A previous meta-analysis found that Fok I polymorphism was associated with TB risk with significant heterogeneity [ 20 , 21 ]. However, they did not stratify by HIV status.…”

Section: Introductionmentioning

confidence: 99%

Vitamin D Receptor Gene FOKI Polymorphism Contributes to Increasing the Risk of HIV-Negative Tuberculosis: Evidence from a Meta-Analysis

Tang

Ding

et al. 2015

PLoS ONE

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“…Gp91phox, encoded by CYBB ranked second in Table 1, is an essential subunit of NADPH oxidase complex. Alterations in macrophage function, such as defects in NADPH oxidase30 and the vitamin D receptor,31 are known as risk factors for mycobacterial infection. Several studies have shown that mutations in CYBB could result in X-linked chronic granulomatous disease with much higher risk of TB,32–34 which is an immunodeficiency caused by defective activity of NADPH oxidase in phagocytes 33,35.…”

Section: Resultsmentioning

confidence: 99%

<p>The blood transcriptional signature for active and latent tuberculosis</p>

Deng¹,

Liu²,

Fang³

et al. 2019

IDR

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BackgroundAlthough the incidence of tuberculosis (TB) has dropped substantially, it still is a serious threat to human health. And in recent years, the emergence of resistant bacilli and inadequate disease control and prevention has led to a significant rise in the global TB epidemic. It is known that the cause of TB is Mycobacterium tuberculosis infection. But it is not clear why some infected patients are active while others are latent.MethodsWe analyzed the blood gene expression profiles of 69 latent TB patients and 54 active pulmonary TB patients from GEO (Transcript Expression Omnibus) database.ResultsBy applying minimal redundancy maximal relevance and incremental feature selection, we identified 24 signature genes which can predict the TB activation. The support vector machine predictor based on these 24 genes had a sensitivity of 0.907, specificity of 0.913, and accuracy of 0.911, respectively. Although they need to be validated in a large independent dataset, the biological analysis of these 24 genes showed great promise.ConclusionWe found that cytokine production was a key process during TB activation and genes like CYBB, TSPO, CD36, and STAT1 worth further investigation.

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“…The authors showed that African-American individuals with high susceptibility to TB had low serum 25-hydroxyvitamin D levels, leading to inefficient cathelicidin mRNA expression (Liu et al, 2006). Several VDR polymorphisms (FokI, TaqI, BsmI, ApaI) have been found to be associated with TB resistance (Uitterlinden et al, 2004;Sun et al, 2015). A Gambian study has demonstrated that the homozygous T/T TaqI genotype, correlated with higher circulating levels of 1,25(OH) 2 D 3, might be protective against TB (Bellamy et al, 1999).…”

Section: Vitamin D Receptor (Vdr)mentioning

confidence: 99%

Immune response gene polymorphisms in tuberculosis

et al. 2015

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Tuberculosis (TB), an infectious disease caused by Mycobacterium tuberculosis (M.tb), remains a leading public health problem in most parts of the world. Despite the discovery of the bacilli over 100 years ago, there are still many unanswered questions about the host resistance to TB. Although one third of the world's population is infected with virulent M.tb, no more than 5-10% develop active disease within their lifetime. A lot of studies suggest that host genetic factors determine the outcome of M.tb-host interactions, however, specific genes and polymorphisms that govern the development of TB are not completely understood. Strong evidence exists for genes encoding pattern recognition receptors (TLR, CD14), C-type lectins, cytokines/chemokines and their receptors (IFN-γ, TNF-α, IL-12, IL-10, MCP-1, MMP-1), major histocompatibility complex (MHC) molecules, vitamin D receptor (VDR), and proton-coupled divalent metal ion transporters (SLC11A1). Polymorphisms in these genes have a diverse influence on the susceptibility to or protection against TB among particular families, ethnicities and races. In this paper, we review recent discoveries in genetic studies and correlate these findings with their influence on TB susceptibility.

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Vitamin D receptor FokI gene polymorphism and tuberculosis susceptibility: a meta-analysis

Cited by 14 publications

References 34 publications

Vitamin D Receptor Gene FOKI Polymorphism Contributes to Increasing the Risk of HIV-Negative Tuberculosis: Evidence from a Meta-Analysis

Vitamin D Receptor Gene FOKI Polymorphism Contributes to Increasing the Risk of HIV-Negative Tuberculosis: Evidence from a Meta-Analysis

<p>The blood transcriptional signature for active and latent tuberculosis</p>

Immune response gene polymorphisms in tuberculosis

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