scholarly journals Concerted Actions by PIICP, CTXII, and TNF-α in Patients with Juvenile Idiopathic Arthritis

Biomolecules ◽  
2021 ◽  
Vol 11 (5) ◽  
pp. 648
Author(s):  
Katarzyna Winsz-Szczotka ◽  
Kornelia Kuźnik-Trocha ◽  
Iwona Lachór-Motyka ◽  
Wojciech Lemski ◽  
Krystyna Olczyk
Keyword(s):  
Juvenile Idiopathic Arthritis ◽  
Joint Destruction ◽  
Treatment Strategies ◽  
Type Ii Collagen ◽  
Diagnostic Tools ◽  
Type Ii ◽  
Process Indicators ◽  
Tnf Α ◽  
Turnover Markers ◽  
Factor Α

Joint destruction in juvenile idiopathic arthritis (JIA), initiated in the early, preclinical stage of the disease, is diagnosed on the basis of clinical evaluation and radiographic imaging. The determination of circulating cartilage-matrix turnover markers can facilitate the diagnosis and application of better and earlier treatment strategies for JIA. We have shown that 96 JIA patients have elevated levels of procollagen II C-terminal propeptide (PIICP), reflecting the extent of joint cartilage biosynthesis, and C-telopeptide of type II collagen (CTXII), a biomarker of the resorption of this tissue. Patients who did not respond to treatment had particularly high levels of these markers. JIA treatment resulted in the normalization of these markers in remissive patients, but not in those with active JIA. We showed correlations between examined variables and inflammatory process indicators, i.e., C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), and tumor necrosis factor-α (TNF-α). The TNF-α of patients responding to treatment correlated with PIICP, especially in the patients before treatment (r = 0.898, p < 0.001). Significant changes in serum PIICP during JIA therapy suggest its potential diagnostic utility in the monitoring of disease activity and the possibility of its use in assessing treatment towards remission. Understanding changes in type II collagen metabolism over the course of the discussed arthritis may allow the implementation of both new diagnostic tools and new therapeutic strategies in children with JIA.

scholarly journals Telmisartan Mitigates TNF-α-Induced Type II Collagen Reduction by Upregulating SOX-9

ACS Omega ◽  
2021 ◽  
Vol 6 (17) ◽  
pp. 11756-11761
Author(s):  
Xiuying Zhang ◽  
Yanfeng Dong ◽  
Hanyu Dong ◽  
Yanhui Cui ◽  
Qing Du ◽  
...  
Keyword(s):  
Type Ii Collagen ◽  
Type Ii ◽  
Tnf Α

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.

scholarly journals Effect of Marine Phytoplankton (Oceanix) and Undenatured Type II Collagen in Combination with Exercise on Endurance Capacity and Oxidative Stress in Rats

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 1764-1764
Author(s):  
Kazim Sahin ◽  
Cemal Orhan ◽  
Mehmet Tuzcu ◽  
Nurhan Sahin ◽  
Vijaya Juturu
Keyword(s):  
Antioxidant Enzymes ◽  
Proinflammatory Cytokines ◽  
Type Ii Collagen ◽  
Marine Phytoplankton ◽  
Albino Rats ◽  
High Dose ◽  
Endurance Capacity ◽  
Type Ii ◽  
Tnf Α ◽  
Undenatured Type Ii Collagen

Abstract Objectives To study the effect of exercise training alone and or in combination with marine phytoplankton (Oceanix, OCX) and undenatured type II collagen (UCII) supplementation on the endurance capacity, pro-inflammatory markers, and antioxidant defense markers in rats. Methods A total of 28 male Wistar albino rats were randomly divided into four groups (n  =  7) (i) No exercise and no OCX (Control), (ii) Exercise, (iii) Exercise +OCX-I (2.55 mg d/rat) + UC-II (4 mg), iv) Exercise + OCX-2 (5.1 mg d/rat)+UC-II (4 mg). Levels of cholesterol, triglyceride, proinflammatory cytokines (IL-1β, IL-6, TNF-α, COMP, CRP), lactate and malondialdehyde (MDA) levels activities of antioxidant enzymes were determined in all the groups. Results Run to exhaustion (minutes) improved in the OCX + UC-II treated groups. Levels of cholesterol, triglyceride, proinflammatory cytokines (IL-1β, IL-6, TNF-α, COMP, CRP) decreased by OCX + UC-II supplementation. A significant decrease in lactate and malondialdehyde (MDA) levels and an increase in activities of antioxidant enzymes were observed in the combination of exercise and OCX + UC-II groups. Exercise + OCX + UC-II treated had lower TNF-α and IL-1β levels in muscle than exercise and control rats (P &lt; 0.001). Muscle sterol regulatory element-binding protein 1c (SREBP-1c), liver X receptors (LXR), ATP citrate lyase (ACLY) and fatty acid synthase (FAS) levels in the exercise + OCX + UC-II group were lower than all groups (P &lt; 0.05). The effectiveness of the high dose of OCX was more pronounced than the low dose of OCX. Conclusions These results suggest OCX and UC-II with exercise may enhance lipid metabolism by regulation of gene products involved in lipid and antioxidant metabolism including SREBP-1c, -γ, LXR, ACLY and FAS in rats. Funding Sources Lonza.

scholarly journals Interleukin 6 Is Required for the Development of Collagen-induced Arthritis

1998 ◽  
Vol 187 (4) ◽  
pp. 461-468 ◽  
Author(s):  
Tonino Alonzi ◽  
Elena Fattori ◽  
Domenico Lazzaro ◽  
Patrizia Costa ◽  
Lesley Probert ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Interleukin 6 ◽  
Clinical Manifestations ◽  
Inflammatory Cells ◽  
Synovial Fibroblasts ◽  
Type Ii Collagen ◽  
Collagen Induced Arthritis ◽  
Tnf Α ◽  
Cytokine Networks ◽  
Factor Α

Interleukin-6 (IL-6) is overproduced in the joints of patients with rheumatoid arthritis (RA) and, based on its multiple stimulatory effects on cells of the immune system and on vascular endothelia, osteoclasts, and synovial fibroblasts, is believed to participate in the development and clinical manifestations of this disease. In this study we have analysed the effect of ablating cytokine production in two mouse models of arthritis: collagen-induced arthritis (CIA) in DBA/1J mice and the inflammatory polyarthritis of tumor necrosis factor α (TNF-α) transgenic mice. IL-6 was ablated by intercrossing an IL-6 null mutation into both arthritis-susceptible genetic backgrounds and disease development was monitored by measuring clinical, histological, and biochemical parameters. Two opposite responses were observed; while arthritis in TNF-α transgenic mice was not affected by inactivation of the IL-6 gene, DBA/1J, IL-6−/− mice were completely protected from CIA, accompanied by a reduced antibody response to type II collagen and the absence of inflammatory cells and tissue damage in knee joints. These results are discussed in the light of the present knowledge of cytokine networks in chronic inflammatory disorders and suggest that IL-6 receptor antagonists might be beneficial for the treatment of RA.

scholarly journals The Prospects of tumor necrosis factor α inhibitors use in patients with COVID-19

2021 ◽  
Vol 15 (2) ◽  
pp. 89-93
Author(s):  
E. S. Aronova ◽  
B. S. Belov
Keyword(s):  
Clinical Trials ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Randomized Clinical Trials ◽  
Treatment Strategies ◽  
Current Data ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

The review highlights the problem of finding new effective treatment strategies for COVID-19. Tumor necrosis factor α (TNF-α) is considered as a therapeutic target. The theoretical basis for the successful use of TNF-α inhibitors (ITNFα) for the treatment of COVID-19 is presented, as well as data on existing practical developments, including ongoing clinical trials. Two drugs from the group of ITNFα – infliximab and adalimumab – are currently being considered as possible options. The safety issues of ITNFα treatment in patients with immunophaling rheumatic diseases and COVID-19 are discussed. The review also provides current data on vaccination against COVID-19, in particular on the vaccines currently available in Russia, which are at different stages of clinical trials. We conclude that randomized clinical trials of the effectiveness and safety of ITNF-α in patients with the new coronavirus infection are needed. Such trials will promote transition from theoretical speculations to real clinical practice.

scholarly journals The Type II Heat-Labile Enterotoxins LT-IIa and LT-IIb and Their Respective B Pentamers Differentially Induce and Regulate Cytokine Production in Human Monocytic Cells

2004 ◽  
Vol 72 (11) ◽  
pp. 6351-6358 ◽  
Author(s):  
George Hajishengallis ◽  
Hesham Nawar ◽  
Richard I. Tapping ◽  
Michael W. Russell ◽  
Terry D. Connell
Keyword(s):  
Cytokine Production ◽  
Nuclear Factor Κb ◽  
Type I ◽  
Type Ii ◽  
Cytokine Induction ◽  
Heat Labile ◽  
Tnf Α ◽  
A Subunit ◽  
Anti Inflammatory ◽  
Factor Α

ABSTRACT The type II heat-labile enterotoxins, LT-IIa and LT-IIb, exhibit potent adjuvant properties. However, little is known about their immunomodulatory activities upon interaction with innate immune cells, unlike the widely studied type I enterotoxins that include cholera toxin (CT). We therefore investigated interactions of LT-IIa and LT-IIb with human monocytic THP-1 cells. We found that LT-II enterotoxins were inactive in stimulating cytokine release, whereas CT induced low levels of interleukin-1β (IL-1β) and IL-8. However, all three enterotoxins potently regulated cytokine induction in cells activated by bacterial lipopolysaccharide or fimbriae. Induction of proinflammatory (tumor necrosis factor α [TNF-α]) or chemotactic (IL-8) cytokines was downregulated, whereas induction of cytokines with anti-inflammatory (IL-10) or mucosal adjuvant properties (IL-1β) was upregulated by the enterotoxins. These effects appeared to depend on their A subunits, because isolated B-pentameric subunits lacked regulatory activity. Enterotoxin-mediated inhibition of proinflammatory cytokine induction in activated cells was partially attributable to synergism for endogenous production of IL-10 and to an IL-10-independent inhibition of nuclear factor κB (NF-κB) activation. In sharp contrast to the holotoxins, the B pentamers (LT-IIaB and, to a greater extent, LT-IIbB) stimulated cytokine production, suggesting a link between the absence of the A subunit and increased proinflammatory properties. In this regard, the ability of LT-IIbB to activate NF-κB and induce TNF-α and IL-8 was antagonized by the LT-IIb holotoxin. These findings support distinct immunomodulatory roles for the LT-II holotoxins and their respective B pentamers. Moreover, the anti-inflammatory properties of the holotoxins may serve to suppress innate immunity and promote the survival of the pathogen.

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