scholarly journals The effect of the pro-inflammatory cytokine tumor necrosis factor-alpha on human joint capsule myofibroblasts

2010 ◽  
Vol 12 (1) ◽  
pp. R4 ◽  
Author(s):  
Stefan G Mattyasovszky ◽  
Alexander Hofmann ◽  
Christoph Brochhausen ◽  
Ulrike Ritz ◽  
Sebastian Kuhn ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Inflammatory Cytokine ◽  
Joint Capsule ◽  
Necrosis Factor Alpha ◽  
Cytokine Tumor Necrosis Factor ◽  
Factor Alpha ◽  
Necrosis Factor ◽  
Human Joint

scholarly journals INFLUENCE OF AUTOLEUKOCYTE VACCINATION ON ACTIVITY LEVEL OF TUMOR NECROSIS FACTOR ALPHA IN PATIENTS WITH CHRONIC HEPATITIS B

2019 ◽  
Vol 72 (1) ◽  
pp. 31-34
Author(s):  
Alexandr Zinchuk ◽  
Oleksandr Herasun ◽  
Andrij Zadorozhnyi ◽  
Olga Vorozhbyt ◽  
Borys Gerasun
Keyword(s):  
Chronic Hepatitis ◽  
Tumor Necrosis Factor ◽  
Hepatitis B ◽  
Chronic Hepatitis B ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Inflammatory Cytokine ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Necrosis Factor

Introduction: data about influence of intradermal vaccination with native autoleukocytes on activity level of pro-inflammatory cytokine tumor necrosis factor alpha in patients with chronic hepatitis B have been presented in the article. The aim: Based on positive results, obtained from autoleukocyte immunization in patients with psoriasis [14], the aim of our research was to use and study such therapy for reducing the synthesis of pro-inflammatory cytokine TNF-α in patients with chronic hepatitis B (chronic hepatitis B). Materials and methods: Patients with chronic hepatitis B with high level of tumor necrosis factor alpha (≥30pg/ml) were vaccinated with native autoleukocytes (23); simultaneously, the same procedure was performed to patients (11) with low level of this cytokine (5pg/ml). Leukocytes were isolated from heparinized peripheral venous blood of a patient with hepatitis B by centrifuging plasma, obtained after blood precipitation for 140-160 minutes at temperature 370 С. The suspension was resuspended in 1-1.5 ml of a patient’s blood serum and injected into the skin of the back in the dose 0.1 ml. Results: in 30 days after immunization, reduction of tumor necrosis factor alpha was observed in all patients with its high level (100%), in 65.25% of individuals – to 5 pg/ml; in some patients, who had low or average level of pro-inflammatory cytokine, the level individually increased (41.67%). Conclusions: The elaborated method of influence on activity of tumor necrosis factor alpha in patients with chronic hepatitis B is effective and worth implementing into clinical practice.

scholarly journals Osteogenesis Is Improved by Low Tumor Necrosis Factor Alpha Concentration through the Modulation of Gs-Coupled Receptor Signals

2017 ◽  
Vol 37 (8) ◽  
Author(s):  
Simona Daniele ◽  
Letizia Natali ◽  
Chiara Giacomelli ◽  
Pietro Campiglia ◽  
Ettore Novellino ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Osteoblast Differentiation ◽  
Tumor Necrosis ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Cytokine Tumor Necrosis Factor ◽  
Factor Alpha ◽  
High Doses ◽  
Necrosis Factor

ABSTRACT In the early phase of bone damage, low concentrations of the cytokine tumor necrosis factor alpha (TNF-α) favor osteoblast differentiation. In contrast, chronic high doses of the same cytokine contribute to bone loss, demonstrating opposite effects depending on its concentration and on the time of exposure. In the bone microenvironment, TNF-α modulates the expression/function of different G protein-coupled receptors (GPCRs) and of their regulatory proteins, GPCR-regulated kinases (GRKs), thus dictating their final biological outcome in controlling bone anabolic processes. Here, the effects of TNF-α were investigated on the expression/responsiveness of the A2B adenosine receptor (A2BAR), a Gs-coupled receptor that promotes mesenchymal stem cell (MSC) differentiation into osteoblasts. Low TNF-α concentrations exerted a prodifferentiating effect on MSCs, pushing them toward an osteoblast phenotype. By regulating GRK2 turnover and expression, the cytokine impaired A2BAR desensitization, accelerating receptor-mediated osteoblast differentiation. These data supported the anabolic effect of TNF-α submaximal concentration and demonstrated that the cytokine regulates GPCR responses by interfering with the receptor desensitization machinery, thereby enhancing the anabolic responses evoked by A2BAR ligands. Overall, these results indicated that GPCR desensitization plays a pivotal role in osteogenesis and that its manipulation is an effective strategy to favor bone remodeling.

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