• Asian Pacific Journal of Cancer Prevention
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• v.14 no.8
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• pp.4765-4768
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• 2013

Aims: This study was conducted to evaluate the levels of TNF-${\alpha}$, IL-6, IL-8 and VEGF in serum of patients with non- small cell lung cancer, for assessing their possible diagnostic and prognostic roles. Methods: We enrolled 48 patients newly diagnosed with non-small cell lung cancer and 40 healthy controls. TNF- ${\alpha}$, IL-6 and IL-8 levels were measured in the serum of all the subjects with specific radioimmunoassay kits, while EGF was analyzed by sandwich enzyme immunoassay techniques. Results: A statistically significant difference was observed between lung cancer patients and the control group regarding the values of TNF-${\alpha}$, IL-6, IL-8 and VEGF in serum. Moreover, TNF-${\alpha}$, IL-8 and VEGF levels were higher in patients with advanced stages compared to early stages. In addition, higher serum levels of TNF-${\alpha}$, IL-6, IL-8 and VEGF were found in smokers than in non-smokers, both in patients and controls. Conclusion: Serum levels of TNF-${\alpha}$, IL-6, IL-8 and VEGF were all elevated in lung cancer patients, suggesting that inflammatory cytokines could be jointly used as a screening tool. Though TNF-${\alpha}$, IL-8 and VEGF levels were related to advanced disease, long-term survival studies of NSCLC patients should be performed to confirm whether they can act as biomarkers of advanced disease. In addition, smoking would be an important contributor to the processes of inflammation and lung cancer.

• Korean Journal of Pharmacognosy
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• v.45 no.3
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• pp.256-261
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• 2014

Bee venom (BV) therapy has been used as a traditional medicine to treat a variety of conditions, such as arthritis, back pain, cancerous tumors, and skin diseases. However, regulatory effects of BV on tumor necrosis factor (TNF)-${\alpha}$-induced HaCaT cell migration or anti-inflammatory have not been explored. In the present study, we investigated the effects of BV on HaCaT cell migration and anti-inflammation. HaCaT cell migration was evaluated by wound-healing assay. The pro-inflammatory cytokines such as TNF-${\alpha}$, interleukin (IL)-$1{\beta}$, and IL-8 were examined by ELISA or Western blotting. BV treatment led to an increase in migration of HaCaT cells for 24 and 48 h. Especially, 10 ng/ml of BV were significantly increased HaCaT cell migration. Also, BV suppressed the secretion of TNF-${\alpha}$, IL-$1{\beta}$, and IL-8 in culture medium with HaCaT cells. In addition, Western blot results demonstrate that BV suppressed the expression of TNF-${\alpha}$ and IL-$1{\beta}$, in HaCaT cells. Especially, 1 or 10 ng/ml of BV markedly decreased the expression of pro-inflammatory cytokines. These results demonstrate the potential of BV for the prevention of skin inflammation induced by TNF-${\alpha}$.

• Clinical and Experimental Reproductive Medicine
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• v.26 no.1
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• pp.97-101
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• 1999

Male genital tract inflammatory conditions may be associated with unexplained infertility. The presence of cytokine such as tumor necrosis factor-alpha (TNF-${\alpha}$) was reported in the semen of infertile men. However, the effect of these cytokines on human sperm function is still unclear. The purpose of this study was to investigate the in-vitro effects of TNF-alpha on human sperm motility with computer assisted sperm analysis. Washed sperm from 16 normal men were incubated without and with TNF-${\alpha}$ (0.1, 10, 1000 ng/ml). The changes of parameters of sperm motility were recorded at different time intervals (0, 5, 24 hour). There was no significant change of parameters of sperm motility in the incubation with TNF-${\alpha}$. It is suggested that TNF-${\alpha}$ alone does not interfere with the sperm motility and more studies are needed.

• Journal of Veterinary Clinics
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• v.31 no.6
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• pp.469-476
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• 2014

The aims of this study were to explore the effects of conjugated linoleic acid (CLA) on reactive oxygen species (ROS) production in lipopolysaccharide (LPS)-naïve and LPS-stimulated RAW 264.7 macrophages and to examine whether these effects affect the regulation of tumor necrosis factor-alpha (TNF-${\alpha}$) production, and nuclear factor-kappa B (NF-${\kappa}B$) and peroxisome proliferator-activated receptor gamma ($PPAR{\gamma}$) activation. Trans-10, cis-12(t10c12)-CLA increased the production of ROS, as well as TNF-${\alpha}$ in LPS-naïve RAW 264.7 cells. The CLA-induced TNF-${\alpha}$ production was suppressed by treatment of diphenyleneiodonium chloride (DPI), a NADPH oxidase inhibitor. In addition, CLA enhanced the activities of NF-${\kappa}B$ and $PPAR{\gamma}$ in LPS-naïve RAW 264.7 cells, and this effect was abolished with DPI treatment. LPS treatment increased ROS production, whereas CLA reduced LPS-induced ROS production. LPS increased both TNF-${\alpha}$ production and NF-${\kappa}B$ activity, whereas t10c12-CLA reduced TNF-${\alpha}$ production and NF-${\kappa}B$ activity in LPS-stimulated RAW 264.7 cells. DPI treatment suppressed LPS-induced ROS production and NF-${\kappa}B$ activity. Moreover, DPI enhanced the inhibitory effects of t10c12-CLA on TNF-${\alpha}$ production and NF-${\kappa}B$ activation in LPS-stimulated RAW 264.7 cells. However, neither t10c12-CLA nor DPI affected $PPAR{\gamma}$ activity in LPS-stimulated RAW 264.7 cells. Taken together, these data indicate that t10c12-CLA induces TNF-${\alpha}$ production by increasing ROS production in LPS-naïve RAW 264.7 cells, which is mediated by the enhancement of NF-${\kappa}B$ activity via $PPAR{\gamma}$ activation. By contrast, t10c12-CLA suppresses TNF-${\alpha}$ production by inhibiting ROS production and NF-${\kappa}B$ activation via a $PPAR{\gamma}$-independent pathway in LPS-stimulated RAW 264.7 cells. These results suggest that t10c12-CLA can modulate TNF-${\alpha}$ production and NF-${\kappa}B$ activation through formation of ROS in RAW 264.7 macrophages.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• v.32 no.1
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• pp.8-18
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• 2006

Purpose: The purpose of this study was to verify that the expressions of angiogenin, transforming growth factor-beta(TGF-${\beta}$), vascular endothelial growth factor(VEGF), human apurinic/apyrimidinic endonuclease(APEX) and tumor necrosis factor-alpha(TNF-${\alpha}$) were associated with the tumorigenesis of the oral squamous cell carcinoma(OSCC). Materials and Methods: Fifty-one samples of OSCC and fifteen normal oral mucosae were obtained to analyze the expression levels of above five factors. mRNA expressions were quantified by the quantitative competitive PCR(QC-PCR) method. After 2% agarose gel electrophoresis stained with ethidium bromide, the concentration of mRNA was calculated by a digital image analysis system. The expression levels of angiogenin, TGF-${\beta}$, VEGF, APEX and TNF-${\alpha}$ were compared by unpaired Student's t-tests between cancer and normal tissues. We analyzed statistically to find the cut-off values that would be useful as diagnostic markers, and the linear regression analysis between every two factors of these five factors by SAS system. Results: All of these five factors (angiogenin: P<0.0037, TGF-${\beta}$: P<0.0001, VEGF: P<0.0102, APEX: P<0.0023, TNF-${\alpha}$: P<0.0074) were significantly correlated with OSCC. In the analysis to find the cut-off values for the diagnosis, we could not find any value that had a reasonable sensitivity and specificity. In the linear regression analysis, there were correlations between angiogenin and TNF-${\alpha}$, TGF-${\beta}$ and VEGF, TGF-${\beta}$ and APEX, TGF-${\beta}$ and TNF-${\alpha}$, VEGF and APEX, VEGF and TNF-${\alpha}$, APEX and TNF-${\alpha}$. Conclusion: Our results suggest that not only angiogenin, TGF-${\beta}$, VEGF, APEX and TNF-${\alpha}$ are significantly associated with the tumorigenesis, but also the close relationship between these factors might enhance the tumorigenesis of OSCC. We can not find clinical availability for diagnosis.

• Tuberculosis and Respiratory Diseases
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• v.54 no.2
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• pp.199-209
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• 2003

Background : Unexplained weight loss, which commonly occurs in patients with chronic obstructive pulmonary disease(COPD), is important because weight loss is an independent risk factor of mortality and morbidity in these patients. Leptin is known to play an important role in regulating body weight. In addition, the tumor necrosis factor($TNF-{\alpha}$) might also play a potential role in the weight loss experienced in chronic wasting disease. The aim of this study was to determine the influence of plasma leptin and the circulating $TNF-{\alpha}$ system to the difference in the body compositions in patients with COPD. Methods : Spirometry, body composition analysis and the plasma concentrations of leptin, $TNF-{\alpha}$ and a soluble TNF receptor (STNF-R55, -R75) were measured in 31 patients with chronic bronchitis and 10 patients with emphysema. The COPD subtype was classified by the transfer coefficient of carbon monoxide, DLco/VA. Results : The circulating levels of leptin were significantly lower in those patients with emphysema($108.5{\pm}39.37pg/ml$) than those with chronic bronchitis($180.9{\pm}57.7pg/ml$). The circulating levels of sTNF-R55 were significantly higher in the emphysema patients($920.4{\pm}116.4pg/ml$) than in those with chronic bronchitis($803.2{\pm}80.8pg/ml$). There was no relationship between the circulating leptin levels and the activated TNF system in patients with chronic bronchitis and emphysema. However, the circulating leptin levels correlated well with the BMI and fat mass in both patient groups. Conclusion : These results suggest that the weight loss noted in emphysema patients may be associated with the activation of the $TNF-{\alpha}$ system rather than the plasma leptin level.

• YAKHAK HOEJI
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• v.46 no.6
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• pp.477-481
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• 2002

Ellagitannins have been reported to enhance the immune system. In this study, the effects of pedunculagin on langerhans cells were examined. Pedunculagin, an ellagitannin from Alnus hirsuta var. microphylla. Betulaceae, is a novel immunomodulator. Langerhans cell are known as the potent antigen presenting cell and elicit the Contact Hypersensitivity (CHS) response by presenting Ag to trafficking Ag-specific T cells within the skin. For determining the effects af pedunculagin on murine langerhans cell, the expression of TNF-$\alpha$ mRNA was examined by RT-PCR. As a result, the expression of TNF-$\alpha$ mRNA was upregulated by pedunculagin. These results suggest that pedunculagin enhances TNF-$\alpha$ and could be used as an immunomodulator in skin immune system.

• Journal of Life Science
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• v.12 no.2
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• pp.57-60
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• 2002

Apoptosis of vascular smooth muscle cell is observed in the vascular diseases such as atherosclerosis and restenosis. The death of vascular smooth muscle cells can be induced by cytokines and activation of Fas-pathways. It is widely accepted that apoptosis occurs without inflammation. There are, however, reports that apoptosis is not silent. Vascular smooth muscle cells dying by Fas-pathway secreted inflammatory cytokines including monocyte chemoattractant protein-1. This study have investigated whether apoptosis is associated with potent inflammatory cytokine tumor tumor necrosis factor (TNF)-${\alpha}$. The cells which undergo apoptosis by expressing FADD in the absence of tetracycline expressed and secreted TNF-${\alpha}$. When the level of TNF-${\alpha}$ transcript was investigated, dying smooth muscle cells exhibited transcriptional activation of TNF-${\alpha}$. The data indicate that dying vascular smooth muscle cells contribute to inflammation by expressing inflammatory cytokines. The present study suggests that apoptosis could not be silent in certain pathological situations.

• Parasites, Hosts and Diseases
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• v.49 no.2
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• pp.191-194
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• 2011

Sparganosis is a tissue invading helminthiasis infecting intermediate hosts, including humans. Strong immune responses are expected to occur in early phases of infection. Thus, we investigated cytokine expressions in splenic dendritic cells and in sera after experimental infection of mice. In splenic dendritic cells, TNF-${\alpha}$ and IL-$1{\beta}$ expression peaked at week 1 and week 3 post -infection (PI), respectively, and also early phase (week 2 PI) depressed cytokine expression was noticed. Serum IL-$1{\beta}$ concentration increased significantly at week 2 PI and peaked at week 6 PI, and that of TNF-${\alpha}$ peaked at week 6 PI. These results showed that pro-inflammatory cytokines, TNF-${\alpha}$ and IL-$1{\beta}$, are chronologically regulated in mouse sparganosis.

• Journal of Acupuncture Research
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• v.24 no.3
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• pp.197-205
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• 2007

Objectives : Tumor necrosis factor-${\alpha}$(TNF ${\alpha}$) is a proinflammatory cytokine involved in the pathogenesis of rheumatoid arthritis. This study was designed to investigate the relation between TNF-${\alpha}$ gene polymorphism and rheumatoid arthritis in Korean population. Methods : This study was carried out on 103 rheumatoid arthritis patients who fulfilled the American College of Rheumatology 1987 revised criteria for rheumatoid arthritis and 208 healthy control subjects. Blood samples from all subjects were obtained for DNA extraction. The extracted DNA was amplified by polymerse chain reaction(PCR). PCR products were visualized by 2% agarose gel electrophoresis. We investigated the genotyping of TNF-${\alpha}$ by using Pyrosequencing. Results: The genotypes of TNF-${\alpha}$ gene were GG, AG and AA. While the distribution of TNF-${\alpha}$ polymorphism in control subjects was 92.31%, 7.21%, 0.48% respectively, in rheumatoid arthritis patients was 93.20%, 6.80%, 0.00%(GG, AG, AA). There was no statistical significant allelic frequency difference between control and rheumatoid arthritis groups. Conclusions : We concluded that there was no significant association between TNF-${\alpha}$ gene polymorphism and rheumatoid arthritis. However, the findings of this study need to be confirmed in more patients and further studies.