&lt;p&gt;Effect of TNF-α &lt;em&gt;−308G/A (rs1800629)&lt;/em&gt; Promoter Polymorphism on the Serum Level of TNF-α Among Iraqi Patients with Generalized Vitiligo&lt;/p&gt;

Ahmed, Ronak; Sharif, Dana Ahmed; Jaf, Mohammad; Amin, Dashty Mohammed

doi:10.2147/ccid.s272970

Cited by 12 publications

(15 citation statements)

References 44 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…22 The role TNFα plays in inhibiting melanogenesis is thought to be through lowering the intracellular levels of both tyrosinase and tyrosinase-related protein 1 which is a melanosomal glycoprotein engaged in the process of melanogenesis and also in inhibition of melanocyte death. 23 The statistically significant positive correlation found in our work between SAA levels and both VASI scores and duration of vitiligo among the studied patients indicates that SAA is a good marker for vitiligo severity. This correlation might be explained that increased SAA levels in vitiligo patient cause further increase in proinflammatory factors such as IL-17, IL-8, TNFα, IL-12, IL-6, and matrix metalloproteinases, which, in turn, confirms the role of SAA as a key inflammatory mediator in pathogenesis of vitiligo and its antimelanocyte reactivity which leads to both more aggressive and more progressive forms of vitiligo.…”

Section: Ta B L Esupporting

confidence: 62%

Unraveling the relation between vitiligo, Interleukin 17, and serum amyloid A

Ahmed

Mikhael

El-Fallah

et al. 2022

J of Cosmetic Dermatology

View full text Add to dashboard Cite

The exact etiopathogenesis of vitiligo is still a matter of debade. The development of white macules is the clinical hallmark of vitiligo due to the selective loss of melanocytes. The prevalence of the disease is around 0.5-1.0% worldwide. 1 Vitiligo may be a psychologically distressing condition, especially in people with darker skin because it is more evident on them. It seems to be genetically transmitted in a polygenic/multifactorial way. It has been suggested that immunological factors, oxidative stress, and/or sympathetic neurogenic disruption are the etiology; however, this is still up for debate. 2

show abstract

Section: Ta B L Esupporting

confidence: 62%

Unraveling the relation between vitiligo, Interleukin 17, and serum amyloid A

Ahmed

Mikhael

El-Fallah

et al. 2022

J of Cosmetic Dermatology

View full text Add to dashboard Cite

show abstract

“…Numerous studies indicate the role of TNF-α in the pathogenesis of proliferative diabetic retinopathy and the wet form of age-related macular degeneration -such conclusions lead to information about the increase in the concentration of protein necrosis factoralpha in the aqueous fluid of the eye among patients with such pathologies [20]. The gene expressing this biological agent contains one of the most studied polymorphisms that is likely to affect the expression of TNF-α, located in the promoter region of the gene in front of the transcription initiator, at 308 nucleotides, and known as G-308A (rs1800629) [1]. All allelic variations of this polymorphism have different ability to pathogenic activation, in particular: the wild genotype GG has a complex effect, without changing the risk of associated pathological processes.…”

Section: Discussionmentioning

confidence: 99%

Investigation of the effect of TNF-α on damage to retinal pigment epithelial cells in age-related macular degeneration

Малачкова

Masa’deh

2022

Rep. of Morph.

View full text Add to dashboard Cite

Oxidative stress alters cellular homeostasis and elicits a cellular response that depends on the severity and type of damage: some cells activate defense mechanisms designed to ensure survival; the other, provided that the defense mechanisms are inhibited, triggers alternative signaling pathways that lead to apoptosis, necrosis, pyroptosis, autophagy, and so on. However, the exact cause of such damage and induction of oxidative stress, including the associated oxidative effects around pigment epithelial cells in the context of the onset and progression of age-related macular degeneration – one of the world’s most common eye diseases with blindness, remains unclear. Therefore, in the course of the study we turned to key biogenetic points of regulation of inflammation and apoptosis, in particular TNF. The aim of the work is to shed light on the role of TNF as a genetic determinant that can initiate and influence the course of age-related macular degeneration. For this purpose, the main pathognomonic markers of the morphological structure of the macula were determined in 291 persons with age-related macular degeneration and in 105 persons without ophthalmic pathology, using optical coherence tomography to confirm or exclude the diagnosis of the disease. To detect polymorphism of the TNF gene, we used the method of real-time PCR diagnostics on the BioRad CFX 96 amplifier using LiTech reagents. Statistical processing of the results was performed using Hardy-Weinberg equilibrium, Kruskal-Wallis method, logistic regression analysis and construction of the ROC curve to determine the AUC range and sensitivity and specificity values. The study revealed a significant difference in the distribution of mutant genotypes between patients with both forms of AMD and the control group. There was also a statistically significant effect of mutant allele A on the development of both "dry" (OR = 3.40; 95.0 %; CI = 1.90-6.07, p<0.001) and "wet" form of AMD (OR = 4.78; 95.0 % CI 2.65-8.64, p<0.001), and in the analysis of mutant genotypes it was found that the GA genotype increases the chances of "dry" and "wet" forms of the disease by 3.13 and 4.74 times, respectively, while AA – 5 times, regardless of the form of the disease. confirms the influence of TNF gene polymorphism on the occurrence and progression of age-related macular degeneration. In the analysis of ROC-curves and AUC regions, it was found that all mutant genotypes have a significant effect on the occurrence of age-related macular degeneration (p<0.05). However, the obtained values of sensitivity and specificity, especially in the AA genotype in both "dry" (17.9 % and 95.8 %, respectively) and "wet" (18.2 % and 95.8 %, respectively) forms of age-related macular degeneration indicate a low chance of error-free confirmation of the diagnosis. a disease that may be associated with multifactorial disease and requires further research.

show abstract

“…Nevertheless, the results are still rather inconsistent. We have reviewed a number of studies reporting the levels of TNF-α in different populations of mixed adults across the different genotypes for some of those variants, predominantly for the −308 G/A [ 41 , 42 , 137 , 139 , 140 , 141 , 142 , 143 , 144 ] ( Table S7 ). As repeatedly indicated in the previous sections, we found a very high intra-subgroup (genotype) variability with most CV% values well above 30% and in many cases >100%.…”

Section: The Influence Of Genetic Variants On Tnf-α Levelsmentioning

confidence: 99%

An Exploratory Critical Review on TNF-α as a Potential Inflammatory Biomarker Responsive to Dietary Intervention with Bioactive Foods and Derived Products

Quarta

Massaro

Carluccio

et al. 2022

Foods

View full text Add to dashboard Cite

This review collects and critically examines data on the levels of tumour necrosis factor-alpha (TNF-α) in lean, overweight and obese subjects, and the effects of intervention with different foods and food products containing bioactive constituents in overweight/obese individuals. We additionally explore the influence of different single nucleotide polymorphisms (SNPs) on TNF-α levels and compare the response to food products with that to some anti-obesity drugs. Our aim was to provide an overview of the variability, consistency, and magnitude of the reported effects of dietary factors on TNF-α, and to envisage the reliability of measuring changes in the levels of this cytokine as a biomarker responsive to food intervention in association with the reduction in body weight. Regarding the circulating levels of TNF-α, we report: (i) a large intra-group variability, with most coefficients of variation (CV%) values being ³30% and, in many cases, >100%; (ii) a large between-studies variability, with baseline TNF-α values ranging from <1.0 up to several hundred pg/mL; (iii) highly variable effects of the different dietary approaches with both statistically significant and not significant decreases or increases of the protein, and the absolute effect size varying from <0.1 pg/mL up to ≈50 pg/mL. Within this scenario of variability, it was not possible to discern clear differentiating limits in TNF-α between lean, overweight, and obese individuals or a distinct downregulatory effect on this cytokine by any of the different dietary approaches reviewed, i.e., polyunsaturated fatty acids (PUFAs), Vitamin-D (VitD), mixed (micro)nutrients, (poly)phenols or other phytochemicals. Further, there was not a clear relationship between the TNF-α responses and body weight changes. We found similarities between dietary and pharmacological treatments in terms of variability and limited evidence of the TNF-α response. Different factors that contribute to this variability are discussed and some specific recommendations are proposed to reinforce the need to improve future studies looking at this cytokine as a potential biomarker of response to dietary approaches.

show abstract

<p>Effect of TNF-α <em>−308G/A (rs1800629)</em> Promoter Polymorphism on the Serum Level of TNF-α Among Iraqi Patients with Generalized Vitiligo</p>

Cited by 12 publications

References 44 publications

Unraveling the relation between vitiligo, Interleukin 17, and serum amyloid A

Unraveling the relation between vitiligo, Interleukin 17, and serum amyloid A

Investigation of the effect of TNF-α on damage to retinal pigment epithelial cells in age-related macular degeneration

An Exploratory Critical Review on TNF-α as a Potential Inflammatory Biomarker Responsive to Dietary Intervention with Bioactive Foods and Derived Products

Contact Info

Product

Resources

About