scholarly journals Evaluation of Interleukin-1α, Interleukin-10, Tumor Necrosis Factor-α and transforming Growth Factor-β in the Serum of Patients with Pemphigus Vulgaris

2014 ◽  
Vol 15 (6) ◽  
pp. 746-749 ◽  
Author(s):  
Faezeh Khozeimeh ◽  
Omid Savabi ◽  
Masih Esnaashari
Keyword(s):  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Transforming Growth Factor ◽  
Pemphigus Vulgaris ◽  
Transforming Growth Factor Β ◽  
Interleukin 10 ◽  
Tnf Α ◽  
Interleukin 1Α ◽  
Factor Α ◽  
Necrosis Factor

ABSTRACT Pemphigus is an autoimmune blistering disease characterized by a loss of cell adhesion result in acantholysis. Genetic factors and immunologic factors such as cytokines particularly IL-1α, IL-10, TNF-α, and TGF-β may counterpart to developing of Pemphigus. The aim of this study was to evaluate. The concentration of IL-1α, IL-10, TNF-α, TGF-α in serum of pemphigus vulgaris (PV) patients and normal individuals. Material and methods In this analytic and descriptive study 25 patients with pemphigus vulgaris (in active phase) and 25 healthy persons were examined. Serum samples of two groups were obtained and the level of IL-1α, IL-10, TNF-α and TGF-β were measured by ELISA technique. The data were analyzed statistically by independent T test (α = 0/05). Results All cytokines tested, showed higher concentration in patient's sera comparing to healthy control individuals. The level of IL-1α (p = 0.004), TNF-α (p = 0.008) and TGF-β (p = 0.009) were statistically different in two experimental groups, There was no significant difference in IL-10 level (p = 0.605). Conclusion Cytokines such as IL-1α, IL-10, TNF-α and TGF-β probably have a role in pathogenesis of PV. Further comprehensive studies are suggested to confirm these findings. How to cite this article Khozeimeh F, Savabi O, Esnaashari M. Evaluation of Interleukin-1α, Interleukin-10, Tumor Necrosis Factor-α and transforming Growth Factor-β in the Serum of Patients with Pemphigus Vulgaris. J Contemp Dent Pract 2014;15(6):746-749.

Regulation of Murine Protein C Gene Expression In Vivo: Effects of Tumor Necrosis Factor-α, Interleukin-1, and Transforming Growth Factor-β

1999 ◽  
Vol 82 (10) ◽  
pp. 1297-1301 ◽  
Author(s):  
Takayoshi Shimokawa ◽  
Tetsuhito Kojima ◽  
David Loskutoff ◽  
Hidehiko Saito ◽  
Koji Yamamoto
Keyword(s):  
Growth Factor ◽  
Protein C ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Transforming Growth Factor ◽  
Interleukin 1 ◽  
Transforming Growth Factor Β ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

SummaryProtein C is a precursor of the anticoagulant serine protease, activated protein C, which inhibits coagulation factors Va and VIIIa. Although the liver appears to be the primary site of protein C synthesis, we previously demonstrated that the kidney and male reproductive organs also expressed abundant protein C mRNA in the mouse. In the present study, we further investigated the effects of tumor necrosis factor-α (TNF-α), interleukin-1 (IL-1), and transforming growth factor-β (TGF-β) on the expression of protein C mRNA in the principal producing organs, i.e., the liver, kidney, and testis. Both quantitative reverse transcription-PCR assay and in situ hybridization analysis revealed that TNF-α decreased protein C mRNA expression in the liver, kidney, and testis. IL-1 also down-regulated protein C mRNA expression in the liver and testis, but not in the kidney. In contrast, TGF-β unchanged the expression level of protein C mRNA in these three organs. These observations suggest that TNF-α and IL-1 may contribute to an increase in the procoagulant potential by down-regulation of protein C synthesis in the tissues during inflammatory processes.

scholarly journals The Effect of Azadirachta indica leaves extract on Transforming Growth Factor-β and Tumor Necrosis Factor-α in a Plasmodium berghei infected Mice model

2021 ◽  
Vol 7 (1) ◽  
pp. 42
Author(s):  
Zainabur Rahmah
Keyword(s):  
Azadirachta Indica ◽  
Plasmodium Berghei ◽  
Tumor Necrosis ◽  
Leaf Extract ◽  
Tumor Necrosis Factor Α ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Malaria is a health problem for the world's population and is predominantly located in tropical and subtropical areas. The three countries with the most malaria cases are India (58%), followed by Indonesia (20%), then Myanmar (16%). This study aims to determine the effect of neem leaf extract on increasing TGF-β expression and decreasing TNF-α expression in mice infected with Plasmodium berghei. In this study there were four groups, namely Treatment 1 (in Plasmodium berghei infection without therapy). Treatment 2 (in Plasmodium berghei infection and treated with Azadirachta indica leaf extract at a dose of 0.25 mg / g BW). Treatment 3 = (in Plasmodium berghei infection and therapy with Azadirachta indica leaves at a dose of 0.5 mg / g BW). Treatment 4 = (in Plasmodium berghei infection and treated with Azadirachta indica leaves at a dose of 1 mg / g BW). TGF-β examination by elisa method and TNF-α by immunohistochemistry. Data analysis using SEM (Structural Equation Modeling) The results of treatment 1 and 2 showed a decrease in plasma TGF-β expression (t = 1.13; tcount = 1.93; ≥ttabel = 1.96) and spleen (tcount = 1.53; tcount = 1.45; ≥ttabel = 1.96) but there was an increase in spleen TNF-α expression (tcount = 1.77; tcount = 1.00; ≥ttabel = 1.96). Groups 3 and 4 showed an increase in plasma TGF-β expression (tcount = 5.13; tcount = 2.42; ≥ttable = 1.96) and spleen (tcount = 2.00; tcount = 1.97; ≥ttabel = 1.96) but there was a decrease in spleen TNF-α expression (tcount = 2.03; tcount = 2.11; ≥ttabel = 1.96). Conclusion: Azadirachta indica leaf therapy can increase TGF-β expression and decrease TNF-α expression in the spleen. Keywords: Azadirachta indica ethanol extract, transforming growth factor- β, tumor necrosis factor-α

Exposure to febrile temperature modifies endothelial cell response to tumor necrosis factor-α

2001 ◽  
Vol 90 (1) ◽  
pp. 90-98 ◽  
Author(s):  
Jeffrey D. Hasday ◽  
Douglas Bannerman ◽  
Sirhan Sakarya ◽  
Alan S. Cross ◽  
Ishwar S. Singh ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Gm Csf ◽  
Tnf Α ◽  
Neutrophil Adherence ◽  
Endothelial Cell Response ◽  
Factor Α ◽  
Necrosis Factor

Fever is an important regulator of inflammation that modifies expression and bioactivity of cytokines, including tumor necrosis factor (TNF)-α. Pulmonary vascular endothelium is an important target of TNF-α during the systemic inflammatory response. In this study, we analyzed the effect of a febrile range temperature (39.5°C) on TNF-α-stimulated changes in endothelial barrier function, capacity for neutrophil binding and transendothelial migration (TEM), and cytokine secretion in human pulmonary artery endothelial cells (EC). Permeability for [14C]BSA tracer was increased by treatment with TNF-α, and this effect was augmented by incubating EC at 39.5°C. Treating EC with 2.5 U/ml TNF-α stimulated an increase in subsequent neutrophil adherence and TEM. Incubating EC at 39.5°C caused a 30% increase in TEM but did not modify the enhancement of neutrophil adherence or TEM by TNF-α treatment. Analysis of cytokine expression in EC cultures exposed to TNF-α at either 37° or 39.5°C revealed three patterns of temperature and TNF-α responsiveness. Granulocyte-macrophage colony stimulating factor (GM-CSF) and interleukin (IL)-8 were not detectable in untreated EC but were increased after TNF-α exposure, and this increase was enhanced at 39.5°C. IL-6 expression was also increased with TNF-α exposure, but IL-6 expression was lower in 39.5°C EC cultures. Transforming growth factor-β1was constitutively expressed, and its expression was not influenced either by TNF-α or exposure to 39.5°C. These data demonstrate that clinically relevant shifts in body temperature might cause important changes in the effects of proinflammatory cytokines on the endothelium.

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