Tumor necrosis factor gene polymorphisms are associated with silicosis: a systemic review and meta-analysis

Zhang, Min; Peng, Linglong; Xue-lei, JI; Yang, Haibing; Zha, Ri-Sheng; Gui, Guo-Ping

doi:10.1042/bsr20181896

Cited by 12 publications

(16 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…4,9,22,23 Of the six studies analyzed, five evaluated TNF-α concentrations and one investigated the presence of the -308G/A polymorphism, which is a G to A mutation at the -308 position in the promoter region, and is associated with higher levels of TNFα. 13 Despite the fact that these studies are difficult to compare because different fluids were used to measure the concentration of this interleukin, all lead us to reflect on the possibility of developing a more targeted treatment. Two articles 16,18 found a significant difference in TNF-α levels of patients compared to (20), indicating that this interleukin level is higher in patients with greater disability.…”

Section: Discussionmentioning

confidence: 99%

“…12 The single nucleotide polymorphism (SNP) -308G/A TNF-α rs1800629 is characterized by the replacement of guanine (G) with adenine (A) in the promoter region of the gene, which leads to a greater production of this interleukin. 13 Only a few studies have evaluated the presence of interleukins and genetic polymorphisms in TMD patients, but they have provided important results regarding the role of tumor necrosis factor. This has pointed to the possibility of the inclusion of this immune-inflammatory marker of immunity in the evaluation of Dental Press J Orthod.…”

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

TNF-α levels and presence of SNP-308G/A of TNF-α gene in temporomandibular disorder patients

Campello

Lima

Fernandes

et al. 2022

Dental Press J. Orthod.

View full text Add to dashboard Cite

Introduction: Temporomandibular disorder (TMD) refers to a group of conditions that compromise the harmonious movement and function of the temporomandibular joint, masticatory muscles, and associated structures. The etiopathogenesis of TMD is multifactorial but not well-understood, with the role of genetic factors still being unclear. Objective: This review aims to summarize the results of studies that evaluated TNF-α levels and the -308G/A TNF-α polymorphism in TMD patients. This study emphasizes the importance of a more selective treatment involving TNF-α inhibitors that can potentially reduce inflammation and pain, and improve quality of life. Methods: The MEDLINE/PubMed database, Cochrane Library, and Web of Science database were searched for case-control studies published until September 2020 that compared levels of TNF-α or presence of its -308G/A polymorphism in TMD patients and healthy individuals. Results: Six case-control studies were identified with a total of 398 TMD patients, aged between 12 and 78 years. The control group consisted of 149 subjects, aged between 18 and 47 years. The occurrence of TMD was predominant in females. Majority of studies found high TNF-α levels in TMD patients, compared to the control group. One of these studies found a positive correlation between the GA genotype and the development of TMD. Conclusion: Majority of the TMD patients showed elevated TNF-α levels, and a possible explanation for this could be the presence of the -308G/A polymorphism.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

TNF-α levels and presence of SNP-308G/A of TNF-α gene in temporomandibular disorder patients

Campello

Lima

Fernandes

et al. 2022

Dental Press J. Orthod.

View full text Add to dashboard Cite

show abstract

“…Studies have demonstrated that TNF-α manufacture is managed at the transcriptional level 9 , and a G-to-A mutation in the −238, −308 promoter area is linked by an raise in TNF-α manufacture 10 . Furthermore, in spite of the fact that TNF-α promoter have four particular point mutations of G to A are distinguished at the -163, -238, -308, and -376 locales, respectively 11,12 , which may influence TNF -α expression 13 , investigations have shown the SNPs at -238 and -308 are associated with the happened and development of silicosis 8,10,14 . thus, we suppose that polymorphisms in the TNF-α (-308) promoter region is associated with respiratory inflammation risk in concrete laborers.…”

Section: Introductionmentioning

confidence: 99%

Correlation of TNF 308 Polymorphisms and Susceptibility to Respiratory Disease

Dulaimi¹,

Rabee²

2021

Indian Journal of Forensic Medicine & Toxicology

View full text Add to dashboard Cite

To estimate the association of TNF-α 308 SNPs with the risk of respiratory disease in Iraqi concrete laborers. 49 concrete laborers and 40 healthy people were taken on our investigation. Technology of Amplification refractory mutational system-polymerase chain reaction (ARMS-PCR) was used to testify single nucleotide polymorphism (SNP) of TNF-α gene. Enzyme-linked immunosorbent assay (ELISA) technique was utilized to measurement the amount of TNF-α protein. odds ratios (ORs) with 95% confidence intervals (CIs) were utilized to estimate the strength of association. Testing for Hardy-Weinberg (H-W) equilibrium revealed both laborers and control showed significant variation in the distribution of TNF-α-308 genotypes (p ≤0.05). Both genotypic and allelic frequency of rs1800629 show in significant difference between concrete laborers and healthy controls. Nevertheless the frequency of A allele was insignificantly increase in laborers (20%) than in controls (14%) (P = 0.077; OR = 1.61; 95% CI = 0.72 to 3.58). After analyzing the relationship between TNF-α serum levels of laborers and genotype of TNF-α-308G/A, we detected the laborers that carrying the GA and AA genotypes had significantly higher levels of TNF-α compared to GG genotype carriers of rs1800629 ( P< 0.01). Consequently, our information proposed that TNF-α-308G/A variation was linked to risk of respiratory disease in concrete laborers. Moreover, we also identified TNF-α-308 A allele was the risk factor for concrete laborers in Iraqi population.

show abstract

“…Yucesoy et al (2001), based on the results obtained from a case-control study involving male Caucasian underground miners (325 cases and 164 controls), found a strong association between silicosis incidence and polymorphisms of the TNF-a gene. Similarly, based on the results of a meta-analysis involving 1990 silicosis and 1898 healthy controls, Zhang et al (2019) concluded that TNF-a polymorphisms are associated with susceptibility to silicosis. Nevertheless, contrary to the findings of these reports, there are studies that failed to demonstrate an association between silicosis and TNF-a polymorphisms (Qu et al, 2007;Wu et al, 2008).…”

mentioning

confidence: 99%

Tobacco Smoke Exposure Exacerbated Crystalline Silica-Induced Lung Toxicity in Rats

Sager

Umbright

Mustafa

et al. 2020

Toxicological Sciences

View full text Add to dashboard Cite

Smoking may modify the lung response to silica exposure including cancer and silicosis. Nevertheless, the precise role of exposure to tobacco smoke (TS) on the lung response to crystalline silica (CS) exposure and the underlying mechanisms need further clarification. The objectives of the present study were to determine the role of TS on lung response to CS exposure and the underlying mechanism(s). Male Fischer 344 rats were exposed by inhalation to air, CS (15 mg/m3, 6 hrs/day, 5 days), TS (80 mg/m3, 3 hrs/day, twice weekly, 6 months), or CS (15 mg/m3, 6 hrs/day, 5 days) followed by TS (80 mg/m3, 3 hrs/day, twice weekly, 6 months). The rats were euthanized 6 months and 3 weeks following initiation of the first exposure and the lung response was assessed. Silica exposure resulted in significant lung toxicity as evidenced by lung histological changes, enhanced neutrophil infiltration, increased LDH levels, enhanced oxidant production, and increased cytokine levels. The TS exposure alone had only a minimal effect on these toxicity parameters. However, the combined exposure to TS and CS exacerbated the lung response, compared to TS or CS exposure alone. Global gene expression changes in the lungs correlated with the lung toxicity severity. Bioinformatic analysis of the gene expression data demonstrated significant enrichment in functions, pathways, and networks relevant to the response to CS exposure which correlated with the lung toxicity detected. Collectively our data demonstrated an exacerbation of CS-induced lung toxicity by TS exposure and the molecular mechanisms underlying the exacerbated toxicity.

show abstract

Tumor necrosis factor gene polymorphisms are associated with silicosis: a systemic review and meta-analysis

Cited by 12 publications

References 29 publications

TNF-α levels and presence of SNP-308G/A of TNF-α gene in temporomandibular disorder patients

TNF-α levels and presence of SNP-308G/A of TNF-α gene in temporomandibular disorder patients

Correlation of TNF 308 Polymorphisms and Susceptibility to Respiratory Disease

Tobacco Smoke Exposure Exacerbated Crystalline Silica-Induced Lung Toxicity in Rats

Contact Info

Product

Resources

About