TNF -308G &gt; A promoter polymorphism (rs1800629) and outcome from critical illness

Paskulin, Diego D’Ávila; Fallavena, Paulo Roberto Vargas; Paludo, Francis Jackson O.; Borges, Thiago J.; Picanço, Juliane Bentes; Dias, Fernando Suparregui; Alho, Clarice Sampaio

doi:10.1016/s1413-8670(11)70181-7

Cited by 17 publications

(9 citation statements)

References 44 publications

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“…The frequency distribution of the A allele observed in our study (13.83%) was similar to that observed in previous studies in the Brazilian population (12–16%) [59–61]. According to data from the 1000 Genomes project, the frequency of the A allele is similar between Europeans (13%) and Africans (12%).…”

Section: Discussionsupporting

confidence: 89%

Frequency ofTNFA,INFG, andIL10Gene Polymorphisms and Their Association with MalariaVivaxand Genomic Ancestry

Furini

Cassiano

Capobianco

et al. 2016

Mediators of Inflammation

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Polymorphisms in cytokine genes can alter the production of these proteins and consequently affect the immune response. The trihybrid heterogeneity of the Brazilian population is characterized as a condition for the use of ancestry informative markers. The objective of this study was to evaluate the frequency of -1031T>C, -308G>A and -238G>A TNFA, +874 A>T IFNG and -819C>T, and -592C>A IL10 gene polymorphisms and their association with malaria vivax and genomic ancestry. Samples from 90 vivax malaria-infected individuals and 51 noninfected individuals from northern Brazil were evaluated. Genotyping was carried out by using ASO-PCR or PCR/RFLP. The genomic ancestry of the individuals was classified using 48 insertion/deletion polymorphism biallelic markers. There were no differences in the proportions of African, European, and Native American ancestry between men and women. No significant association was observed for the allele and genotype frequencies of the 6 SNPs between malaria-infected and noninfected individuals. However, there was a trend toward decreasing the frequency of individuals carrying the TNF-308A allele with the increasing proportion of European ancestry. No ethnic-specific SNPs were identified, and there was no allelic or genotype association with susceptibility or resistance to vivax malaria. Understanding the genomic mechanisms by which ancestry influences this association is critical and requires further study.

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Section: Discussionsupporting

confidence: 89%

Frequency ofTNFA,INFG, andIL10Gene Polymorphisms and Their Association with MalariaVivaxand Genomic Ancestry

Furini

Cassiano

Capobianco

et al. 2016

Mediators of Inflammation

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“…These studies were published between 1999 and 2015. Fourteen studies were performed in Caucasians [ 22 , 25 – 26 , 28 – 30 , 32 – 34 , 36 – 37 , 40 – 41 , 43 ], 12 in Asians [ 11 , 13 – 16 , 19 – 20 , 24 , 31 , 38 – 39 , 44 ], and the remainder in populations of mixed or unknown ethnicity [ 12 , 17 – 18 , 21 , 23 , 27 , 35 , 42 ]. In contrast, the most recent systematic review and meta-analysis of associations between the −308G/A polymorphism and sepsis contained 25 studies involving 2,977 patients [ 10 ].…”

Section: Resultsmentioning

confidence: 99%

Tumor necrosis factor-α −308 G/A polymorphism and risk of sepsis, septic shock, and mortality: an updated meta-analysis

et al. 2017

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BackgroundThe -308G/A polymorphism in the gene encoding tumor necrosis factor-α (TNF-α) has been implicated in sepsis risk in many studies but with variable results. This study aimed to comprehensively assess the evidence of association between this polymorphism and risk of sepsis and sepsis-related mortality.Materials and MethodsPubMed, EMBASE and other databases were searched to identify relevant studies, and data were analyzed using Review Manager 5.0 and STATA 12.0.ResultsData from 34 publications involving 12,284 subjects were meta-analyzed. Combined analysis revealed an association between TNF-α -308G/A gene polymorphism and risk of sepsis (AA+GA vs. GG, OR 1.35, 95% CI 1.10–1.67, P = 0.005). This association was observed in the Caucasian subgroup (OR 1.50, 95% CI 1.13–2.00, P = 0.006), but not in the Asian subgroup. Across the entire study population, the polymorphism was also significantly related to septic shock risk (OR 1.52, 95% CI 1.18–1.95, P = 0.001) but not to sepsis-related mortality (OR 0.99, 95% CI 0.71–1.40, P = 0.97).ConclusionsThis meta-analysis suggests that the -308G/A gene polymorphism in the TNF-α gene may contribute to risk of sepsis and septic shock, but not risk of mortality.

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“…Although susceptibility for presenting an adverse clinical course (i.e., sepsis, septic shock, multiples organ failure, or death) varies due to different degrees of inflammatory response [30], genetic factors of the host may influence the nature and intensity of this response. The present study is the first to demonstrate that the polymorphisms in genes related to the inflammatory response may, in some manner, be influencing the risk of infection by influenza A/H1N1 virus and of death from this illness.…”

Section: Discussionmentioning

confidence: 99%

“…Elevated levels of pro-inflammatory cytokines and chemokines (e.g., TNFα, IFNγ, IL-1, IL-6, IL-8, IL-9, IL-12 IL-15, and IL-17) have been found, up to ten days after the onset of symptoms, in the plasma of patients with acute respiratory distress syndrome (ARDS) caused by influenza A/H1N1 [9,10,14]. The genes that code for these molecules are polymorphic and certain alleles have been associated with susceptibility to various diseases that cover a wide range of pathologies, from infectious to oncological, including pulmonary and systemic diseases [15-30]. The role that the polymorphisms of the genes encoding these cytokines play in the severity of the disease is not clear.…”

Section: Introductionmentioning

confidence: 99%

Pandemic influenza A/H1N1 virus infection and TNF, LTA, IL1B, IL6, IL8, and CCLpolymorphisms in Mexican population: a case–control study

et al. 2012

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BackgroundSome patients have a greater response to viral infection than do others having a similar level of viral replication. Hypercytokinemia is the principal immunopathological mechanism that contributes to a severer clinical course in cases of influenza A/H1N1. The benefit produced, or damage caused, by these cytokines in severe disease is not known. The genes that code for these molecules are polymorphic and certain alleles have been associated with susceptibility to various diseases. The objective of the present study was to determine whether there was an association between polymorphisms of TNF, LTA, IL1B, IL6, IL8, and CCL1 and the infection and severity of the illness caused by the pandemic A/H1N1 in Mexico in 2009.MethodsCase–control study. The cases were patients confirmed with real time PCR with infection by the A/H1N1 pandemic virus. The controls were patients with infection like to influenza and non-familial healthy contacts of the patients with influenza. Medical history and outcome of the disease was registered. The DNA samples were genotyped for polymorphisms TNF rs361525, rs1800629, and rs1800750; LTA rs909253; IL1B rs16944; IL6 rs1818879; IL8 rs4073; and CCL1 rs2282691. Odds ratio (OR) and the 95% confidence interval (95% CI) were calculated. The logistic regression model was adjusted by age and severity of the illness in cases.ResultsInfection with the pandemic A/H1N1 virus was associated with the following genotypes: TNF rs361525 AA, OR = 27.00; 95% CI = 3.07–1248.77); LTA rs909253 AG (OR = 4.33, 95% CI = 1.82–10.32); TNF rs1800750 AA (OR = 4.33, 95% CI = 1.48–12.64); additionally, LTA rs909253 AG showed a limited statistically significant association with mortality (p = 0.06, OR = 3.13). Carriers of the TNF rs1800629 GA genotype were associated with high levels of blood urea nitrogen (p = 0.05); those of the TNF rs1800750 AA genotype, with high levels of creatine phosphokinase (p=0.05). The IL1B rs16944 AA genotype was associated with an elevated number of leukocytes (p <0.001) and the IL8 rs4073 AA genotype, with a higher value for PaO2 mm Hg.ConclusionThe polymorphisms of genes involved in the inflammatory process contributed to the severity of the clinical behavior of infection by the pandemic influenza A/H1N1 virus.

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TNF -308G > A promoter polymorphism (rs1800629) and outcome from critical illness

Cited by 17 publications

References 44 publications

Frequency ofTNFA,INFG, andIL10Gene Polymorphisms and Their Association with MalariaVivaxand Genomic Ancestry

Frequency ofTNFA,INFG, andIL10Gene Polymorphisms and Their Association with MalariaVivaxand Genomic Ancestry

Tumor necrosis factor-α −308 G/A polymorphism and risk of sepsis, septic shock, and mortality: an updated meta-analysis

Pandemic influenza A/H1N1 virus infection and TNF, LTA, IL1B, IL6, IL8, and CCLpolymorphisms in Mexican population: a case–control study

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