TNF-α -238, -308, -863 polymorphisms, and brucellosis infection

Eskandari-Nasab, Ebrahim; Moghadampour, Mehdi; Sepanjnia, Adel

doi:10.1016/j.humimm.2015.11.010

Cited by 11 publications

(9 citation statements)

References 43 publications

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“…Similar results were reported by Eskandari-Nasab and his colleagues who stated that the TNF-α-308 A allele or GA heterozygosity were associated with an increased risk of brucellosis (Eskandari-Nasab et al, 2016). Furthermore, few other studies showed a significant association between the TNF-α-308 (A/A) genotype and brucellosis (Caballero et al, 2000b;Davoudi et al, 2006;Reza et al, 2009).…”

Section: Discussionsupporting

confidence: 77%

Study the Impact of T-helper 1 Cytokine (TNF-α) Polymorphisms on Susceptibility/Resistance to Brucellosis in Makkah Region

Ismael¹,

Mergani²,

Mostafa³

et al. 2016

American Journal of Infectious Diseases

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Polymorphisms in the regulatory regions of cytokine genes may not only increase susceptibility to some infectious diseases but also affect the course and prognosis of the disease. TNF-α is considered an important Th1 cytokines that plays critical roles in control of Brucella infection and in macrophage activation. In this study, we are going to analyze the relationship of two polymorphisms in TNF-α and the inherited susceptibility/resistance to brucellosis in population of Makkah region. A cases-control association study was conducted in 69 individuals with human Brucellosis and 112 healthy individuals. Genotyping of TNF-308G>A and -857C>T polymorphism in both patients and healthy controls was done by PCR-RFLP method and were assessed for potential associations with susceptibility for human brucellosis and their mode of penetrance. The findings indicate an increased risk of TNF-α-308 A allele for human brucellosis reliable with the recessive genetic model of penetrance (Odd Ratio: 3.222, 95% CI: 1.008-5.702, P = 0.018). There is no association between susceptibility of human brucellosis and TNF-α-857 C/T polymorphism was observed. The protective role of TNF-α-857 C/T polymorphism against human brucellosis in this study population could not be excluded.

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Section: Discussionsupporting

confidence: 77%

Study the Impact of T-helper 1 Cytokine (TNF-α) Polymorphisms on Susceptibility/Resistance to Brucellosis in Makkah Region

Ismael¹,

Mergani²,

Mostafa³

et al. 2016

American Journal of Infectious Diseases

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“…Blood samples were collected by withdrawal of 5 ml venous blood from each individual involved in this study into sterile EDTA‐containing tubes. DNA was extracted using salting‐out method as described previously Eskandari‐Nasab, Moghadampour, and Sepanj‐Nia (), Sepanjnia, Eskandari‐Nasab, Moghadampour, Tahmasebi, and Dahmardeh (). The quality of the isolated DNA was examined by electrophoresis on 1% agarose gel, quantified spectrophotometrically and stored at −20°C till further use.…”

Section: Methodsmentioning

confidence: 99%

HLA‐G gene 14‐bp deletion variant protects Iranian subjects against chronic hepatitis B infection

Eskandari-Nasab

Dahmardeh

Safdari

et al. 2017

Int J Immunogenetics

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To investigate whether 14-bp Ins/Del polymorphism in HLA-G gene is associated with the risk of chronic hepatitis B (CHB) infection. This study was performed on a total of 396 individuals including 199 CHB patients and 197 healthy subjects from a south-east Iranian population. We genotyped 14-bp Ins/Del polymorphism in the HLA-G gene using polymerase chain reaction method. The results of our study revealed that the HLA-G 14-bp deletion polymorphism was associated with a reduced risk of CHB at both allele and genotypic levels. The 14-bp Del allele and Ins/Del genotype were more frequent in control group than in CHB patients (37% vs 28% for Del allele with OR = 0.68 and p-value = .015; 73% vs 52% for Ins/Del genotype with OR = 0.43 and p-value = .001) and both were protective factors against CHB. However, no difference was found in the distribution of HLA-G 14-bp genotypes among subjects with varied levels of HBV DNA or hepatic enzymes (p > .05). Our findings, for the first time, suggest that the HLA-G 14-bp Ins/Del polymorphism may be a marker for genetic susceptibility to CHB infection.

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“…can stimulate the secretion of inflammatory cytokines, e.g., interleukins (ILs), interferon-gamma (IFN-γ) and tumor necrosis factor-alpha (TNF-α). 2,10,11 IFN-γ is a crucial cytokine for the control of Brucella infection in hosts and is also a significant mediator in conferring protection against Brucella infection. The ultimate result of the activation of macrophages with IFN-γ, which is secreted by T helper-1 cells, is suppressing the reproduction of intracellular Brucella organisms and restoring the patient to health.…”

Section: Introductionmentioning

confidence: 99%

“…Like IFN-γ, TNF-α also is a vital mediator for the clearance of brucellosis infection from a host. 11 Genetic polymorphisms in cytokine genes can potentially modify the expression and/or biological activity of cytokines. Studies conducted to date have confirmed the connection between cytokine gene polymorphisms and brucellosis disease status in various populations.…”

Section: Introductionmentioning

confidence: 99%

“…Studies conducted to date have confirmed the connection between cytokine gene polymorphisms and brucellosis disease status in various populations. 2,[11][12][13][14][15][16] The IFN-γ +874 A/T (rs2430561) and UTR5644 A/T polymorphisms, as well as the TNF-α −308 G/A (rs1800629) and −238 G/A (rs361525), are 4 SNP loci which affect the transcriptional regulation of IFN-γ and TNF-α. These 4 SNPs have been investigated for their association with the occurrence of brucellosis in different populations.…”

Section: Introductionmentioning

confidence: 99%

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The relationship between IFN-γ and TNF-α gene polymorphisms and brucellosis: Meta-analysis

Eskandari-Nasab¹,

Moghadampour²

2018

Adv Clin Exp Med

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TNF-α -238, -308, -863 polymorphisms, and brucellosis infection

Cited by 11 publications

References 43 publications

Study the Impact of T-helper 1 Cytokine (TNF-α) Polymorphisms on Susceptibility/Resistance to Brucellosis in Makkah Region

Study the Impact of T-helper 1 Cytokine (TNF-α) Polymorphisms on Susceptibility/Resistance to Brucellosis in Makkah Region

HLA‐G gene 14‐bp deletion variant protects Iranian subjects against chronic hepatitis B infection

The relationship between IFN-γ and TNF-α gene polymorphisms and brucellosis: Meta-analysis

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TNF-α -238, -308, -863 polymorphisms, and brucellosis infection

Cited by 11 publications

References 43 publications

Study the Impact of T-helper 1 Cytokine (TNF-&alpha;) Polymorphisms on Susceptibility/Resistance to Brucellosis in Makkah Region

Study the Impact of T-helper 1 Cytokine (TNF-&alpha;) Polymorphisms on Susceptibility/Resistance to Brucellosis in Makkah Region

HLA‐G gene 14‐bp deletion variant protects Iranian subjects against chronic hepatitis B infection

The relationship between IFN-γ and TNF-α gene polymorphisms and brucellosis: Meta-analysis

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Study the Impact of T-helper 1 Cytokine (TNF-α) Polymorphisms on Susceptibility/Resistance to Brucellosis in Makkah Region

Study the Impact of T-helper 1 Cytokine (TNF-α) Polymorphisms on Susceptibility/Resistance to Brucellosis in Makkah Region