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

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.

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

Galician Medical Journal ◽

10.21802/gmj.2017.4.12 ◽

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.

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

Ophthalmic Research ◽

10.1159/000513586 ◽

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.

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

Molecular and Cellular Biology ◽

10.1128/mcb.01117-15 ◽

2016 ◽

Vol 36 (9) ◽

pp. 1342-1353 ◽

Cited By ~ 10

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.

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

Molecular and Cellular Biology ◽

10.1128/mcb.01538-06 ◽

2006 ◽

Vol 26 (24) ◽

pp. 9244-9255 ◽

Cited By ~ 43

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.

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Comparative Analysis of Lipopolysaccharide-Induced Tumor Necrosis Factor Alpha Activity in Serum and Lethality in Mice and Rabbits Pretreated with the Staphylococcal Superantigen Toxic Shock Syndrome Toxin 1

Infection and Immunity ◽

10.1128/iai.69.11.7169-7172.2001 ◽

2001 ◽

Vol 69 (11) ◽

pp. 7169-7172 ◽

Cited By ~ 37

Author(s):

Martin M. Dinges ◽

Patrick M. Schlievert

Keyword(s):

Tumor Necrosis Factor ◽

Tumor Necrosis Factor Alpha ◽

Tumor Necrosis ◽

Host Susceptibility ◽

Necrosis Factor Alpha ◽

Lethal Effects ◽

Tnf Α ◽

Factor Alpha ◽

Toxic Shock Syndrome Toxin ◽

Necrosis Factor

ABSTRACT Host susceptibility to lipopolysaccharide (LPS) is correlated with the levels of circulating tumor necrosis factor alpha (TNF-α) that develop in response to circulating LPS. Mice are resistant, relative to rabbits, to the lethal effects of LPS. This study indicates that mice and rabbits are equally sensitive to the lethal effects of circulating TNF-α but that mice are more resistant than rabbits to the induction of circulating TNF-α by LPS.

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Major Outer Membrane Protein Omp25 of Brucella suis Is Involved in Inhibition of Tumor Necrosis Factor Alpha Production during Infection of Human Macrophages

Infection and Immunity ◽

10.1128/iai.69.8.4823-4830.2001 ◽

2001 ◽

Vol 69 (8) ◽

pp. 4823-4830 ◽

Cited By ~ 62

Author(s):

Véronique Jubier-Maurin ◽

Rose-Anne Boigegrain ◽

Axel Cloeckaert ◽

Antoine Gross ◽

Maria-Teresa Alvarez-Martinez ◽

...

Keyword(s):

Tumor Necrosis Factor ◽

Tumor Necrosis Factor Alpha ◽

Tumor Necrosis ◽

Macrophage Infection ◽

Necrosis Factor Alpha ◽

Human Macrophages ◽

Tnf Α ◽

Brucella Suis ◽

Factor Alpha ◽

Necrosis Factor

ABSTRACT Brucella spp. can establish themselves and cause disease in humans and animals. The mechanisms by whichBrucella spp. evade the antibacterial defenses of their host, however, remain largely unknown. We have previously reported that live brucellae failed to induce tumor necrosis factor alpha (TNF-α) production upon human macrophage infection. This inhibition is associated with a nonidentified protein that is released into culture medium. Outer membrane proteins (OMPs) of gram-negative bacteria have been shown to modulate macrophage functions, including cytokine production. Thus, we have analyzed the effects of two major OMPs (Omp25 and Omp31) of Brucella suis 1330 (wild-type [WT] B. suis) on TNF-α production. For this purpose, omp25and omp31 null mutants of B. suis(Δomp25 B. suis and Δomp31 B. suis, respectively) were constructed and analyzed for the ability to activate human macrophages to secrete TNF-α. We showed that, in contrast to WTB. suis or Δomp31 B. suis, Δomp25 B. suis induced TNF-α production when phagocytosed by human macrophages. The complementation of Δomp25 B. suis with WT omp25 (Δomp25-omp25 B. suis mutant) significantly reversed this effect: Δomp25-omp25 B. suis-infected macrophages secreted significantly less TNF-α than did macrophages infected with the Δomp25 B. suismutant. Furthermore, pretreatment of WT B. suis with an anti-Omp25 monoclonal antibody directed against an epitope exposed at the surface of the bacteria resulted in substancial TNF-α production during macrophage infection. These observations demonstrated that Omp25 of B. suis is involved in the negative regulation of TNF-α production upon infection of human macrophages.

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In silico studies for the interaction of tumor necrosis factor-alpha (TNF-α) with different saponins from Vietnamese ginseng (Panax vietnamesis)

Biophysics and Physicobiology ◽

10.2142/biophysico.13.0_173 ◽

2016 ◽

Vol 13 (0) ◽

pp. 173-180 ◽

Cited By ~ 6

Author(s):

Oanh T. P. Kim ◽

Manh D. Le ◽

Hoang X. Trinh ◽

Hai V. Nong

Keyword(s):

Tumor Necrosis Factor ◽

Tumor Necrosis Factor Alpha ◽

In Silico ◽

Tumor Necrosis ◽

Necrosis Factor Alpha ◽

Tnf Α ◽

Factor Alpha ◽

Necrosis Factor

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Gamma Interferon and Lipopolysaccharide Interact at the Level of Transcription To Induce Tumor Necrosis Factor Alpha Expression

Infection and Immunity ◽

10.1128/iai.69.5.2847-2852.2001 ◽

2001 ◽

Vol 69 (5) ◽

pp. 2847-2852 ◽

Cited By ~ 18

Author(s):

Julia Y. Lee ◽

Kathleen E. Sullivan

Keyword(s):

Tumor Necrosis Factor ◽

Tumor Necrosis Factor Alpha ◽

Tumor Necrosis ◽

Gamma Interferon ◽

Necrosis Factor Alpha ◽

Rnase Protection ◽

Tnf Α ◽

Factor Alpha ◽

Ifn Γ ◽

Necrosis Factor

ABSTRACT Lipopolysaccharide (LPS) is a very potent inducer of tumor necrosis factor alpha (TNF-α) expression from monocytes and macrophages. Another inflammatory cytokine, gamma interferon (IFN-γ), can potentiate the effects of LPS, but the mechanism is not thoroughly understood. Previous reports emphasized the ability of IFN-γ to upregulate CD14 expression (the receptor for LPS), and nearly all studies have utilized sequential stimulation with IFN-γ followed by LPS to exploit this phenomenon. This study demonstrates that IFN-γ can upregulate the effect of LPS at the level of transcription. Human monoblastic Mono-Mac-6 cells produced up to threefold-greater levels of TNF-α when simultaneously stimulated with LPS and IFN-γ compared to treatment with LPS alone. RNase protection studies showed a similar increase in RNA beginning as early as within 30 min. The synthesis of TNF-α mRNA in IFN-γ- and LPS-treated Mono-Mac-6 cells was also temporally prolonged even though the message turnover rate was identical to that seen in LPS stimulated cells. The modulatory effect of IFN-γ may be mediated by Jak2.

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