Association of Tumor Necrosis Factor-alpha and Interleukin-6 Gene Polymorphisms with Preeclampsia

2016 ◽  
Vol 5 (02) ◽  
pp. 4774
Author(s):  
Madhavi Puppala* ◽  
V. Lakshmi Kalpana ◽  
Anuradha A ◽  
M. Sushma ◽  
G. Sudhakar ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Confidence Interval ◽  
Odds Ratio ◽  
Gene Polymorphisms ◽  
Tumor Necrosis ◽  
Control Group ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

Preeclampsia is a pregnancy-specific syndrome that may be dangerous especially to the fetus. Different cytokines have been found to be elevated in women with preeclampsia and may have possible roles in the development of this disorder. Alleles of the interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α) genes are associated with preeclampsia in several studies in different populations. The aim of the present study was to investigate the relationship between IL-6 (G174C) and TNF-α (G-308A) gene polymorphisms with preeclampsia in North Coastal Andhra Pradesh of India. The TNFA (-308 A/G) and IL6 (-674G/C) genotypes were determined in 100 preeclamptic women and 100 normal pregnant women as control group, using allele-specific oligonucleotides-polymerase chain reaction method. Data was analyzed using chi-square and Fisher’s exact tests. TNF-α (G-308A) G/G genotype showed a significantly higher frequency among the preeclamptic group than the control group (odds ratio, 0.4603, 95% confidence interval, (0.2521- 0.8405); P = .005). G/A genotype also showed higher frequency among the preeclamptic group compared to control group (odds ratio, 2.508, 95% confidence interval, ((1.341-4.689); P = .001). IL-6 (G174C) genotype significantly higher frequency among the preeclamptic group than the control group (odds ratio, 0.4603, 95% confidence interval, (0.2521- 0.8405); P = .005).  The present study might suggest a role for TNF-α (G-308A) and -174 GC of IL-6 genotype in the development of preeclampsia; suggesting that they are of differing genetic predisposition/pathophysiology.

scholarly journals Changes in the Levels of Pro-Inflammatory Cytokines in Patients with Generalized Periodontitis and Hypertension, Depending on the Method of Treatment

2017 ◽  
Vol 24 (4) ◽  
Author(s):  
T. Vicharenko ◽  
M. Rozhko
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Interleukin 6 ◽  
Tumor Necrosis ◽  
Control Group ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor ◽  
Pro Inflammatory Cytokines

Inflammatory mediators have an important role in the pathogenesis of periodontal disease. One of the leading mediators of the initiation of the pathological process is interleukin-1 (IL-1) – an endogenous pyrogen, a lymphocyte-activating factor. Numerous pro-inflammatory effects of interleukin-1β (IL-1β) occur in synergy with tumor necrosis factor alpha (TNF-α) and interleukin-6 (IL-6), effects on hematopoiesis, participates in nonspecific anti-infective defense.The objective of the study is to determine levels of interleukin-6 and tumor necrosis factor alpha (TNF-α) in patients with hypertension II stage and generalized periodontitis of the II degree depending on the treatment method.There were examined 30 patients with hypertension of the II stage and with generalized periodontitis of the II degree. Patients’ age ranged from 35 to 54 years. These patients were divided into two groups. The control group included 10 patients without general somatic pathology and with healthy periodontitis of the same age. The result of the analysis of tumor necrosis factor alpha (TNF-α) in patients in the first group before the treatment was 10.69±2.33 pg/ml. After the treatment this indicator was 6.97±1.57 pg/ml (p>0.1) in patients of the first group.In patients of the second group the tumor necrosis factor alpha (TNF-α) was 9.49±2.2 pg/ml; after the treatment according to the offered scheme this figure decreased up to 2.77±0.9 pg/ml (p<0.01). The level of tumor necrosis factor alpha (TNF-α) in the control group was 1.5±0.77 pg/ml.Interleukin-6 was 9.91±2.04 pg/ml before the treatment in the first group. After the treatment according to the standard scheme, the level of interleukin-6 was 6.33±0.97 pg/ml (p>0.1). In the second group, before the treatment the level of  interleukin-6 was 9.65±2.41 pg/ml; after the treatment according to the offered scheme it was 2.62±0.5 pg/ml (p<0.01). In the control group the interleukin-6 level was 2.24±0.51 pg/ml.Analyzing the obtained results after the treatment in both groups we can conclude: after the treatment of generalized periodontitis of the II degree in patients with hypertension of the II stage, indices of pro-inflammatory cytokines decreased and ranged in normal limits; in patients from the second group (who received the offered scheme of treatment -including medicines) indexes of pro-inflammatory cytokines were significantly lower than in patients with the standard treatment scheme; the proposed scheme of treatment is more effective for treatment patients with generalized periodontitis of the II degree and hypertension of the II stage.

scholarly journals Endometrial Flushing Tumor Necrosis Factor Alpha and Interleukin 2 Levels in Women with Polycystic Ovary Syndrome, Leiomyoma and Endometrioma: Comparison with Healthy Controls

2019 ◽  
Vol 79 (05) ◽  
pp. 517-523
Author(s):  
Mustafa Demir ◽  
Senol Kalyoncu ◽  
Onur Ince ◽  
Bulent Ozkan ◽  
Sefa Kelekci ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Polycystic Ovary ◽  
Control Group ◽  
Healthy Controls ◽  
Ovary Syndrome ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

Abstract Introduction An important open question in the literature is whether endometrial receptivity marker levels are different in infertility related diseases than healthy women. The aim of the study is to compare the levels of interleukin two (IL-2) and tumor necrosis factor alpha (TNF-α) during the implantation window in the endometrial flushing fluid of polycystic ovary syndrome (PCOS), endometrioma, leiomyoma patients with healthy controls. Material and Methods In this case control study, after obtaining endometrial flushing fluids at mid-luteal phase of ovulatory women with PCOS (n = 20), endometrioma (n = 19), leiomyoma (n = 20) and healthy controls (n = 20), IL-2 and TNF-α levels were measured using ELISA kits in BioTek ELISA devices. Results Mean TNF-α levels (ng/mL) were similar for the PCOS (305.6, p = 0.220) and the leiomyoma group (246.3, p = 0.502) compared to healthy patients (261.1). However, the levels were higher in the endometrioma group (338.2, p = 0,004) than the control group (261.1) in a statistically significant way. Mean IL-2 levels (ng/mL) were significantly lower in the PCOS (290.9, p = 0.0005), the leiomyoma (282.9, p = 0.0002) and the endometrioma patients (229.5, p = 0.0009) than the control group (416.0). Conclusion Relative to the control group, endometrial flushing fluid TNF-α levels were significantly higher in endometrioma patients and IL-2 levels were significantly lower in PCOS, leiomyoma and endometrioma patients. In benign gynecological diseases, endometrial markers related to infertility seem to show differences in endometrial flushing fluid. Future studies might identify the reference values for these markers, and endometrial markers can be used to diagnose gynecologic disorders causing infertility.

Evaluating the interaction between progesterone, tumor necrosis factor-alpha and cortisol on early loss of transferred embryo in beef cows

2013 ◽  
Vol 93 (2) ◽  
pp. 217-225 ◽  
Author(s):  
M. Mason ◽  
E. J. Cuadra ◽  
T. H. Elsasser ◽  
J. Lopez ◽  
J. Yoonsung
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Beef Cows ◽  
Control Group ◽  
Necrosis Factor Alpha ◽  
Early Loss ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

Mason, M., Cuadra, E. J., Elsasser, T. H., Lopez, J. and Yoonsung, J. 2013. Evaluating the interaction between progesterone, tumor necrosis factor-alpha and cortisol on early loss of transferred embryo in beef cows. Can. J. Anim. Sci. 93: 217–225. Fifty-eight non-lactating cows previously synchronized for estrus were assigned to two treatments to assess the effects of progesterone supplementation and its correlation with tumor necrosis factor-α (TNF-α) and cortisol on the survival of the transferred embryos. On day 7 after exhibiting estrus (day 0), cows in both groups received embryos. In contrast with the control group, animals in the CIDR-group had a controlled internal drug release (CIDR) additionally inserted. Blood samples for progesterone, TNF-α and cortisol analysis were taken immediately before insertion and removal of CIDRs and 7 d after insertion. Progesterone did not differ between the control and the CIDR animals at any day of the study; however, it significantly increased at 7 and 14 d after insertion of the embryos in the control animals, compared with the levels observed in that same experimental group at the time of the transfer. Regardless of the treatment, all pregnant cows experienced a significant increase in progesterone from day 0 to day 7. Progesterone on day 0 was correlated to itself (r=0.46) on day 14 and to TNF-α (r=−0.37) on day 0 in pregnant animals; TNF-α on day 7 was significantly higher in pregnant cows compared with non-pregnant and correlated between day 0 and day 14. These results suggest that high levels of progesterone during the first 14 d after the transfer are indicative of the survival of transferred embryos. Additionally, these data also indicate that the decrease in TNF-α concentration on day 7 after the transfer of embryos may be associated with the low concentrations of progesterone observed in the non-pregnant animals.

scholarly journals Association of tumor necrosis factor-alpha -308 G/A and -238 G/A polymorphism with diabetic retinopathy: a systematic review and updated meta-analysis.

2020 ◽  
Author(s):  
Wenna Gao ◽  
Ruilin Zhu ◽  
liu yang
Keyword(s):  
Diabetic Retinopathy ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Meta Analysis ◽  
Entire Group ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

Background: Mounting evidence has suggested tumor necrosis factor-alpha (TNF-α) can promote the development of diabetic retinopathy (DR), and TNF-α gene variants may influence DR risk. However, the results are quite different. Objectives: To comprehensively address this issue, we performed the meta-analysis to evaluate the association of TNF-α-308 G/A and -238 G/A polymorphism with DR. Method: Data were retrieved in a systematic manner and analyzed using STATA Statistical Software. Crude odds ratios (ORs) with 95% confidence intervals (CIs) were used to assess the strength of associations. Allelic and genotypic comparisons between cases and controls were evaluated. Results: For the TNF-α-308 G/A polymorphism, overall analysis suggested a marginal association with DR [the OR(95%CI) of (GA versus GG), (GA + AA) versus GG, and (A versus G) are 1.21(1.04, 1.41), 1.20(1.03, 1.39), and 1.14(1.01, 1.30), respectively]. And the subgroup analysis indicated an enhanced association among the European population. For the TNF-α-238 G/A polymorphism, there was mild correlation in the entire group [the OR(95%CI) of (GA versus GG) is 1.55(1.14,2.11) ], which was strengthened among the Asian population. Conclusion: The meta-analysis suggested that -308 A and -238 A allele in TNF-α gene potentially increased DR risk and showed a discrepancy in different ethnicities.

Tumor Necrosis Factor-α Production-Enhancing Properties of Novel Adamantylalkylthio Derivatives of Some Heterocyclic Compounds

2005 ◽  
Vol 60 (4) ◽  
pp. 471-475 ◽  
Author(s):  
Barbara Orzeszko ◽  
Tomasz Świtaj ◽  
Anna B. Jakubowska-Mućka ◽  
Witold Lasek ◽  
Andrzej Orzeszko ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Heterocyclic Compounds ◽  
Tumor Necrosis ◽  
The Novel ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Factor Α ◽  
Derivatives Of ◽  
Necrosis Factor

Certain adamantylated heterocycles were previously shown to enhance the secretion of tumor necrosis factor alpha (TNF-α) by murine melanoma cells that have been transduced with the gene for human TNF-α and constitutively expressed this cytokine. The stimulatory potency of those compounds depended, among other factors, on the structure of the linker between the adamantyl residue and the heterocyclic core. In the present study, a series of (1-adamantyl)alkylsulfanyl derivatives of heterocyclic compounds was prepared by alkylation of the corresponding thioheterocyles. Of the novel adamantylalkylthio compounds tested in the aforementioned cell line, 2-(2-adamantan-1-ylethylsulfanyl)- 4-methyl-pyrimidine was found to be the most active

scholarly journals Herpes Simplex Virus 1 E3 Ubiquitin Ligase ICP0 Protein Inhibits Tumor Necrosis Factor Alpha-Induced NF-κB Activation by Interacting with p65/RelA and p50/NF-κB1

2013 ◽  
Vol 87 (23) ◽  
pp. 12935-12948 ◽  
Author(s):  
Jie Zhang ◽  
Kezhen Wang ◽  
Shuai Wang ◽  
Chunfu Zheng
Keyword(s):  
Tumor Necrosis Factor ◽  
Ubiquitin Ligase ◽  
Tumor Necrosis ◽  
Nuclear Translocation ◽  
E3 Ubiquitin Ligase ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor ◽  
Hsv 1

NF-κB plays central roles in regulation of diverse biological processes, including innate and adaptive immunity and inflammation. HSV-1 is the archetypal member of the alphaherpesviruses, with a large genome encoding over 80 viral proteins, many of which are involved in virus-host interactions and show immune modulatory capabilities. In this study, we demonstrated that the HSV-1 ICP0 protein, a viral E3 ubiquitin ligase, was shown to significantly suppress tumor necrosis factor alpha (TNF-α)-mediated NF-κB activation. ICP0 was demonstrated to bind to the NF-κB subunits p65 and p50 by coimmunoprecipitation analysis. ICP0 bound to the Rel homology domain (RHD) of p65. Fluorescence microscopy demonstrated that ICP0 abolished nuclear translocation of p65 upon TNF-α stimulation. Also, ICP0 degraded p50 via its E3 ubiquitin ligase activity. The RING finger (RF) domain mutant ICP0 (ICP0-RF) lost its ability to inhibit TNF-α-mediated NF-κB activation and p65 nuclear translocation and degrade p50. Notably, the RF domain of ICP0 was sufficient to interact with p50 and abolish NF-κB reporter gene activity. Here, it is for the first time shown that HSV-1 ICP0 interacts with p65 and p50, degrades p50 through the ubiquitin-proteasome pathway, and prevents NF-κB-dependent gene expression, which may contribute to immune evasion and pathogenesis of HSV-1.

scholarly journals Analysis of Subcellular RNA Fractions Revealed a Transcription-Independent Effect of Tumor Necrosis Factor Alpha on Splicing, Mediated by Spt5

2016 ◽  
Vol 36 (9) ◽  
pp. 1342-1353 ◽  
Author(s):  
Gil Diamant ◽  
Tal Eisenbaum ◽  
Dena Leshkowitz ◽  
Rivka Dikstein
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Independent Effect ◽  
Necrosis Factor Alpha ◽  
Pol Ii ◽  
Tnf Α ◽  
Factor Alpha ◽  
Induced Genes ◽  
Necrosis Factor

The proinflammatory cytokine tumor necrosis factor alpha (TNF-α) modulates the expression of many genes, primarily through activation of NF-κB. Here, we examined the global effects of the elongation factor Spt5 on nascent and mature mRNAs of TNF-α-induced cells using chromatin and cytosolic subcellular fractions. We identified several classes of TNF-α-induced genes controlled at the level of transcription, splicing, and chromatin retention. Spt5 was found to facilitate splicing and chromatin release in genes displaying high induction rates. Further analysis revealed striking effects of TNF-α on the splicing of 25% of expressed genes; the vast majority were not transcriptionally induced. Splicing enhancement of noninduced genes by TNF-α was transient and independent of NF-κB. Investigating the underlying basis, we found that Spt5 is required for the splicing facilitation of the noninduced genes. In line with this, Spt5 interacts with Sm core protein splicing factors. Furthermore, following TNF-α treatment, levels of RNA polymerase II (Pol II) but not Spt5 are reduced from the splicing-induced genes, suggesting that these genes become enriched with a Pol II-Spt5 form. Our findings revealed the Pol II-Spt5 complex as a highly competent coordinator of cotranscriptional splicing.

scholarly journals HSP70 Induction by ING Proteins Sensitizes Cells to Tumor Necrosis Factor Alpha Receptor-Mediated Apoptosis

2006 ◽  
Vol 26 (24) ◽  
pp. 9244-9255 ◽  
Author(s):  
Xiaolan Feng ◽  
Shirin Bonni ◽  
Karl Riabowol
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Kinase Inhibitor ◽  
Heat Shock Gene ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Primary Fibroblasts ◽  
Factor Alpha ◽  
Necrosis Factor

ABSTRACT ING proteins affect apoptosis, growth, and DNA repair by transducing stress signals such as DNA damage, binding histones, and subsequently regulating chromatin structure and p53 activity. p53 target genes, including the p21 cyclin-dependent kinase inhibitor and Bax, an inducer of apoptosis, are regulated by ING proteins. To identify additional targets downstream of p33ING1 and p32ING2, cDNA microarrays were performed on phenotypically normal human primary fibroblasts. The 0.36% of genes affected by ING proteins in primary fibroblasts were distinct from targets seen in established cells and included the HSP70 heat shock gene, whose promoter was specifically induced >10-fold. ING1-induced expression of HSP70 shifted cells from survival to a death pathway in response to tumor necrosis factor alpha (TNF-α), and p33ING1b protein showed synergy with TNF-α in inducing apoptosis, which correlated with reduced NF-κB-dependent transcription. These findings are consistent with previous reports that HSP70 promotes TNF-α-mediated apoptosis by binding I-κΒ kinase gamma and impairing NF-κB survival signaling. Induction of HSP70 required the amino terminus of ING1b but not the plant homeodomain region that was recently identified as a histone binding domain. Regulation of HSP70 gene expression by the ING tumor suppressors provides a novel link between the INGs and the stress-regulated NF-κB survival pathway important in hypoxia and angiogenesis.

Sign in / Sign up

Export Citation Format

Share Document