Staphylococcal enterotoxin B and tumor-necrosis factor-α-induced relapses of experimental allergic encephalomyelitis: Protection by transforming growth factor-β and interleukin-10

1995 ◽  
Vol 25 (11) ◽  
pp. 3035-3040 ◽  
Author(s):  
Giovanna M. Crisi ◽  
Laura Santambrogio ◽  
Gerald M. Hochwald ◽  
Sidney R. Smith ◽  
Joseph A. Carlino ◽  
...  
Keyword(s):  
Tumor Necrosis ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Interleukin 10 ◽  
Staphylococcal Enterotoxin B ◽  
Allergic Encephalomyelitis ◽  
Enterotoxin B ◽  
Factor Α ◽  
Necrosis Factor ◽  
Experimental Allergic

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.

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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