scholarly journals Brief Report: Anti-Tumor Necrosis Factor α Targets Protein Kinase B/c-Akt-Induced Resistance of Effector Cells to Suppression in Juvenile Idiopathic Arthritis

2013 ◽  
Vol 65 (12) ◽  
pp. 3279-3284 ◽  
Author(s):  
Ellen J. Wehrens ◽  
Sebastiaan J. Vastert ◽  
Gerdien Mijnheer ◽  
Jenny Meerding ◽  
Mark Klein ◽  
...  
Keyword(s):  
Juvenile Idiopathic Arthritis ◽  
Protein Kinase ◽  
Tumor Necrosis Factor ◽  
Induced Resistance ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Protein Kinase B ◽  
Effector Cells ◽  
Factor Α ◽  
Necrosis Factor

scholarly journals FRI0374 PLASMA LEVELS OF 14-3-3 PROTEIN, S100A8/S100A9-PROTEIN, INTERLEUKIN-6, INTERLEUKIN-18, INTERLEUKIN-4, INTERLEUKIN-17, INTERLEUKIN-1Β AND TUMOR NECROSIS FACTOR-Α IN CHRONIC NON-BACTERIAL OSTEOMYEILITIS AND NON-SYSTEMIC JUVENILE IDIOPATHIC ARTHRITIS

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 784.3-784
Author(s):  
M. Kostik ◽  
M. Makhova ◽  
D. Kozlova ◽  
D. Vasilyev ◽  
L. Sorokina ◽  
...  
Keyword(s):  
Juvenile Idiopathic Arthritis ◽  
Tumor Necrosis Factor ◽  
Interleukin 6 ◽  
Plasma Levels ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Systemic Juvenile Idiopathic Arthritis ◽  
Immune Mediated ◽  
Factor Α ◽  
Necrosis Factor

Background:Chronic non-bacterial osteomyelitis (CNO) is an immune-mediated disease associated with cytokine dysbalance.Objectives:The aim of our study was to evaluate the cytokines levels in CNO and compare to juvenile idiopathic arthritis (JIA) – disease with immune-mediated mechanism.Methods:The diagnosis of CNO made with criteria, proposed by Jansson (2007, 2009), after the exclusion of other causes of bone disease [1]. We included 42 patients with NBO, 28 patients with non-systemic juvenile idiopathic arthritis (JIA). We evaluated plasma levels of 14-3-3 protein, S100A8/S100A9-protein, interleukine-6 (IL-6), interleukine-18 (IL-18), interleukine-4 (IL-4), interleukine-17 (IL-17), interleukine-1β (IL-1 β) and tumor necrosis factor-α (TNFα) in 2 groups by the ELISA. Statistical analysis was carried out with Statistica 10.0 software. We utilized descriptive statistics (Me; IQR), Mann-Whitney tests.Results:We have found differences in the proinflammatory biomarkers between CNO, JIA. Patients with NBO had lower levels of studied cytokines, exclude14-3-3-protein, S100A8/S100A9 and interleukin-6 compare to JIA patients (table 1).Table 1.Comparison the cytokine levels between CNO, JIA NParameterNBO (n=42)JIA (n=28)pHemoglobin, g/l112 (104; 124)120 (114.5; 126.0)0.02WBC x 109/l7.9 (7.0; 10.5)8.0 (6.7; 10.0)0.86PLT x 109/l347 (259; 408)336.5 (274.0; 390.5)0.98ESR. mm/h25.0 (9.0; 46.0)8.5 (2.5; 13.0)0.013CRP, mg/l6.1 (0.6; 2.4)1.8 (0.4; 11.9)0.02714-3-3, ng/ml21.4 (18.5; 27.1)19.9 (18.0; 27.8)0.77S100A8/S100A9, ng/ml5.9 (5.2; 6.5)5.9 (5.0; 6.2)0.76IL-6, ng/ml126,2 (112.8; 137.5)132.4 (117.4; 142.9)0.16IL-18, ng/ml270.1 (200.1; 316.1)388.3 (373.9; 405.1)0.0000001IL-4, ng/ml15.3 (11.5; 18.2)18.7 (16.2; 20.2)0.003IL-17, ng/ml83.1 (71.1; 97.3)99.2 (87.3; 115.8)0.003IL-1b, ng/ml47.4 (42.0; 51.3)70.8 (65.3; 73.6)0.0000001TNFa, ng/ml19.4 (17.8; 21.3)23.1 (20.2; 25.9)0.0006Conclusion:Patients with CNO had less proinflammatory activity then JIA patients, besides IL-6 and S100A8/S100A9. Further investigations required for finding new more precise biomarkers and finding possible molecular targets for treatment.This work supported by the Russian Foundation for Basic Research (grant № 18-515-57001)References:[1]Jansson AF, et al. Clinical score for nonbacterial osteitis in children and adults. Arthritis Rheum. 2009;60(4):1152-9.Disclosure of Interests:None declared

Tumor Necrosis Factor-α −308 Genotypes Influence Inflammatory Activity and TNF-α Serum Concentrations in Children with Juvenile Idiopathic Arthritis

2009 ◽  
Vol 36 (4) ◽  
pp. 837-842 ◽  
Author(s):  
ANA FILIPA MOURÃO ◽  
JOANA CAETANO-LOPES ◽  
PAULA COSTA ◽  
HELENA CANHÃO ◽  
MARIA JOSÉ SANTOS ◽  
...  
Keyword(s):  
Juvenile Idiopathic Arthritis ◽  
Tumor Necrosis Factor ◽  
Disease Activity ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Inflammatory Activity ◽  
Serum Concentrations ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Objective.Considering the relevance of tumor necrosis factor-α (TNF-α) in the pathophysiology of juvenile idiopathic arthritis (JIA), it is likely that polymorphisms in its promoter area may be relevant in disease susceptibility and activity. We investigated if clinical measures of JIA activity and TNF-α serum concentrations were associated with TNF-α −308 genotypes.Methods.Portuguese patients with JIA in 5 pediatric rheumatology centers were recruited consecutively, along with a control group of healthy subjects. Demographic and clinical data and blood samples were collected from each patient. DNA was extracted for analysis of TNF-α gene promoter polymorphisms at position −308 by restriction fragment-length polymorphism.Results.One hundred fourteen patients and 117 controls were evaluated; 57% of patients presented the oligoarticular subtype, 25% the polyarticular subtype, 8% the systemic subtype, and 9% had enthesitis-related arthritis and 5% psoriatic arthritis. Twenty-four percent of the patients presented the −308 GA/AA genotypes and 76% the −308 GG genotype, similar to findings in controls. Patients with the −308 GA/AA genotype had higher degree of functional impairment, erythrocyte sedimentation rate, 100-mm visual analog scale score for disease activity, and TNF-α levels compared to those with the −308 GG genotype.Conclusion.TNF-α −308 GA/AA genotypes were found to be related to higher inflammatory activity and worse measures of disease activity in Portuguese patients with JIA. They were not associated with susceptibility to JIA.

Tumor necrosis factor‐α inhibitor‐induced psoriasis in juvenile idiopathic arthritis patients

2019 ◽  
Vol 36 (5) ◽  
pp. 613-617 ◽  
Author(s):  
Daniel Groth ◽  
Maria Perez ◽  
James R. Treat ◽  
Leslie Castelo‐Soccio ◽  
Simona Nativ ◽  
...  
Keyword(s):  
Juvenile Idiopathic Arthritis ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Factor Α ◽  
Necrosis Factor

Tumor necrosis factor-α and ceramide induce cell death through different mechanisms in rat mesangial cells

1999 ◽  
Vol 276 (3) ◽  
pp. F390-F397 ◽  
Author(s):  
Yan-Lin Guo ◽  
Baobin Kang ◽  
Li-Jun Yang ◽  
John R. Williamson
Keyword(s):  
Cell Death ◽  
Protein Kinase ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Mesangial Cells ◽  
Tnf Α ◽  
Induced Apoptosis ◽  
Factor Α ◽  
Necrosis Factor

It has been proposed that ceramide acts as a cellular messenger to mediate tumor necrosis factor-α (TNF-α)-induced apoptosis. Based on this hypothesis, it was postulated that resistance of some cells to TNF-α cytotoxicity was due to an insufficient production of ceramide on stimulation by TNF-α. The present study was initiated to investigate whether this was the case in mesangial cells, which normally are insensitive to TNF-α-induced apoptosis. Our results indicate that although C2ceramide was toxic to mesangial cells, the cell death it induced differed both morphologically and biochemically from that induced by TNF-α in the presence of cycloheximide (CHX). The most apparent effect of C2ceramide was to cause cells to swell, followed by disruption of the cell membrane. It is evident that C2ceramide caused cell death by necrosis, whereas TNF-α in the presence of CHX killed the cells by apoptosis. C2ceramide did not mimic the effects of TNF-α on the activation of c-Jun NH2-terminal protein kinase and nuclear factor-κB transcription factor. Although mitogen-activated protein kinase [extracellular signal-related kinase (ERK)] was activated by both C2ceramide and TNF-α, such activation appeared to be mediated by different mechanisms as judged from the kinetics of ERK activation. Furthermore, the cleavage of cytosolic phospholipase A2during cell death induced by C2ceramide and by TNF-α in the presence of CHX showed distinctive patterns. The present study provides evidence that apoptosis and necrosis use distinctive signaling machinery to cause cell death.

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