scholarly journals Cumulative effect of systemic inflammation and oxidative stress in 40 known cases of active rheumatoid arthritis

2015 ◽  
Vol 1 (1) ◽  
pp. 7 ◽  
Author(s):  
Rahul Saxena ◽  
Shilpa Suneja ◽  
Raj Saxena ◽  
Dilutpal Sharma ◽  
Alok Milton Lal
Keyword(s):  
Rheumatoid Arthritis ◽  
Oxidative Stress ◽  
Antioxidant Enzymes ◽  
Systemic Inflammation ◽  
Inflammatory Diseases ◽  
Cumulative Effect ◽  
Extensive Literature ◽  
Reactive Protein ◽  
Ceruloplasmin Level ◽  
Student’S T

<p class="abstract"><strong>Background:</strong> Oxidative stress has been implicated in the pathophysiology of a number of diseases such as cancer, hypertension and inflammatory diseases. Although previous evidences provided extensive literature about the biological role of antioxidant enzymes in rheumatoid arthritis (RA), there is a paucity of satisfactory explanation regarding the alteration in the level of antioxidant enzymes along with marker of systemic inflammation in RA. The objective of present study was to estimate the level of C-reactive protein (CRP), Superoxide dismutase (SOD), Catalase (CAT), Glutathione peroxidase (GSHPx) and Ceruloplasmin in active RA patients.</p><p class="abstract"><strong>Methods:</strong> 40 patients of either sex (30-50 years age group) suffering from active RA and 40 normal healthy individuals served as control; were included in the study. Above mentioned parameters were estimated using standard methods and data from patients and controls were compared by using Student’s t-test.<strong></strong></p><p class="abstract"><strong>Results:</strong> Erythrocyte SOD, CAT and GSHPx activity were significantly low in RA subjects (P&lt;0.001) whereas plasma Ceruloplasmin level was found to be significantly high (P&lt;0.001) as compared to healthy controls.</p><p><strong>Conclusions:</strong> These findings suggest that combined effect of inflammation and free radical generation is involved in the pathogenesis of active RA, characterized by imbalance in antioxidant enzyme status and enhanced CRP levels, which served as an excellent marker of oxidative stress and systemic inflammation in active RA.</p>

scholarly journals OP0035 ASSESSMENT OF THE INTESTINAL PERMEABILITY IN PATIENTS WITH RHEUMATOID ARTHRITIS USING COLONIC TISSUES AND SERA

2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 19.2-19
Author(s):  
R. Audo ◽  
P. Sanchez ◽  
J. Mielle ◽  
L. Macia ◽  
B. Rivière ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Gut Microbiota ◽  
Intestinal Permeability ◽  
Systemic Inflammation ◽  
Inflammatory Diseases ◽  
Staining Intensity ◽  
Serum Markers ◽  
Before And After ◽  
Colonic Biopsies ◽  
Junction Proteins

Background:Patients with rheumatoid arthritis (RA) have an altered gut microbiota (dysbiosis) (1-3). This microbiota interacts with intestinal epithelium which can lead to an increased intestinal permeability, responsible for the passage of antigens and inflammatory molecules, and can therefore promote systemic inflammation. Gut microbiota tends to normalize with disease control (2), suggesting that systemic inflammation may directly influence the composition of microbiota and the gut barrier. It was shown in many inflammatory diseases that intestinal permeability is impaired, but to date there is very little data in RA.Objectives:In the present study, we evaluate the intestinal permeability in RA patients by analyzing tight junctions in colonic biopsies and serum markers.Methods:Colonic biopsies from 20 RA patients who underwent coloscopy for screening with normal histology were compared with those from 20 age and sex matched controls. ZO-1, occludin and claudin 2 junction proteins were evaluated by immunohistochemistry. The staining intensity was assessed by two blinded independent readers. The serum concentrations of LPS-binding protein (LBP), CD14s and zonulin were evaluated by ELISA in 25 patients naive of DMARDs, 41 patients before and after introduction of a DMARDs and 21 controls. Elevated zonulin in serum indicates an increase in intestinal permeability while LBP and CD14s indicate bacterial translocation.Results:ZO-1 expression was significantly lower in biopsies from patients with RA than controls (mean score ± SD of 1.6 ± 0.56 vs 2.0 ± 0.43; p = 0.01). Age, sex, disease duration and immunological status did not significantly influence the expression of colonic junction proteins. LBP and CD14s were higher in serum from RA patients naive of DMARDs than controls (p = 0.002 and p = 0.003). LBP, CD14s and zonulin levels significantly correlated with DAS28 (r = 0.61, p = 0.005; r = 0.51, p = 0.030 and r = 0.46, p = 0.049, respectively). After treatment, unlike non-responders, LBP and CD14s were significantly reduced in DMARD responders and variations in LBP and CD14s significantly correlated with changes in DAS28 (r = 0.46, p = 0.002 and r = 0, 33 and p = 0.030, respectively).Conclusion:This work is one of the first to explore intestinal permeability in RA and to show altered tight junction in colonic tissue from RA. This increased intestinal permeability appears to be related to the systemic inflammation. Improving the gut microbiota through food or probiotics could enhance the effect of treatments by limiting this amplification loop of inflammation.References:[1]Horta-Baas G, Romero-Figueroa MDS, Montiel-Jarquin AJ, Pizano-Zarate ML, Garcia-Mena J, Ramirez-Duran N. Intestinal Dysbiosis and Rheumatoid Arthritis: A Link between Gut Microbiota and the Pathogenesis of Rheumatoid Arthritis. J Immunol Res. 2017;2017:4835189.[2]Zhang X, Zhang D, Jia H, Feng Q, Wang D, Liang D, et al. The oral and gut microbiomes are perturbed in rheumatoid arthritis and partly normalized after treatment. Nat Med. 2015;21(8):895-905.[3]Maeda Y, Kurakawa T, Umemoto E, Motooka D, Ito Y, Gotoh K, et al. Dysbiosis Contributes to Arthritis Development via Activation of Autoreactive T Cells in the Intestine. Arthritis Rheumatol. 2016;68(11):2646-61.Disclosure of Interests:Rachel Audo: None declared, Pauline Sanchez: None declared, Julie Mielle: None declared, Laurence Macia: None declared, Benjamin Rivière: None declared, Cédric Lukas: None declared, Bernard Combe: None declared, Jacques Morel: None declared, Claire Daien Speakers bureau: Pfizer roche chugai fresenius BMS msd Novartis galapagos, Consultant of: Abivax abbbvie BMS roche chugai, Grant/research support from: Pfizer, roche-chugai, fresenius, msd

scholarly journals Title: Human Serum/Plasma Glycoprotein Analysis by 1H-NMR, an Emerging Method of Inflammatory Assessment

2020 ◽  
Vol 9 (2) ◽  
pp. 354 ◽  
Author(s):  
Fuertes-Martín ◽  
Correig ◽  
Vallvé ◽  
Amigó
Keyword(s):  
1H Nmr ◽  
Systemic Inflammation ◽  
Metabolic Diseases ◽  
Inflammatory Diseases ◽  
Inflammatory Marker ◽  
Point Of View ◽  
Proton Nuclear Magnetic Resonance ◽  
New Paradigm ◽  
Reactive Protein ◽  
Wide Range

Several studies suggest that variations in the concentration of plasma glycoproteins can influence cellular changes in a large number of diseases. In recent years, proton nuclear magnetic resonance (1H-NMR) has played a major role as an analytical tool for serum and plasma samples. In recent years, there is an increasing interest in the characterization of glycoproteins through 1H-NMR in order to search for reliable and robust biomarkers of disease. The objective of this review was to examine the existing studies in the literature related to the study of glycoproteins from an analytical and clinical point of view. There are currently several techniques to characterize circulating glycoproteins in serum or plasma, but in this review, we focus on 1H-NMR due to its great robustness and recent interest in its translation to the clinical setting. In fact, there is already a marker in H-NMR representing the acetyl groups of the glycoproteins, GlycA, which has been increasingly studied in clinical studies. A broad search of the literature was performed showing a general consensus that GlycA is a robust marker of systemic inflammation. The results also suggested that GlycA better captures systemic inflammation even more than C-reactive protein (CRP), a widely used classical inflammatory marker. The applications reviewed here demonstrated that GlycA was potentially a key biomarker in a wide range of diseases such as cancer, metabolic diseases, cardiovascular risk, and chronic inflammatory diseases among others. The profiling of glycoproteins through 1H-NMR launches an encouraging new paradigm for its future incorporation in clinical diagnosis.

scholarly journals Influence of TNF-α inhibition on oxidative stress of rheumatoid arthritis patients

Reumatismo ◽  
2016 ◽  
Vol 67 (3) ◽  
pp. 97 ◽  
Author(s):  
F. Cacciapaglia ◽  
M.G. Anelli ◽  
D. Rizzo ◽  
E. Morelli ◽  
C. Scioscia ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Oxidative Stress ◽  
Health Assessment ◽  
Good Control ◽  
Oxidative Stress Marker ◽  
Reactive Oxygen Metabolites ◽  
Necrosis Factor Alpha ◽  
Reactive Protein ◽  
Tnf Α ◽  
Oxidative Stress Status

The aim of this study was to assess circulating levels of reactive oxygen metabolites (ROMs) as a marker of oxidative stress in rheumatoid arthritis (RA) patients during an anti-tumor necrosis factor alpha (TNF-α) treatment. We enrolled 40 patients with RA (36 females; age 53±13 yrs) treated with different subcutaneously administered TNF-α inhibitors. The oxidative status was determined on the basis of plasma samples taken before, at 24 and 52 weeks of the anti-TNF-α treatment. Hydroperoxide levels were measured using the d-ROMs test, a useful clinically proven oxidative stress marker. During the anti-TNF-α therapy, we observed a significant reduction in serum ROMs levels in RA patients from 33.2±10 mg H2O2/L at baseline to 29.5±7 and 29.3±9 mg H2O2/L, at 24 and 52 weeks, respectively (p&lt;0.05). We also identified a significant correlation between the oxidative stress status and the disease activity score on 28 joints/C-reactive protein and health assessment questionnaire disability index. The results of our study demonstrate that a good control of the disease with anti-TNF-α agents can reduce oxidative stress in RA patients. However, further studies of larger patient cohorts are needed to confirm these preliminary data.

scholarly journals Potential Use ofPlectranthus amboinicusin the Treatment of Rheumatoid Arthritis

2010 ◽  
Vol 7 (1) ◽  
pp. 115-120 ◽  
Author(s):  
Jia-Ming Chang ◽  
Chun-Ming Cheng ◽  
Le-Mei Hung ◽  
Yuh-Shan Chung ◽  
Rey-Yuh Wu
Keyword(s):  
Rheumatoid Arthritis ◽  
Inflammatory Diseases ◽  
Type Ii Collagen ◽  
Pharmacological Action ◽  
Action Mode ◽  
Reactive Protein ◽  
Tnf Α ◽  
Plectranthus Amboinicus ◽  
Potential Use ◽  
Bovine Type

Plectranthus amboinicus(P. amboinicus) is a folk herb that is used to treat inflammatory diseases or swelling symptoms in Taiwan. We investigated therapeutic efficacy ofP. amboinicusin treating Rheumatoid Arthritis (RA) using collagen-induced arthritis animal model. Arthritis was induced in Lewis rats by immunization with bovine type II collagen. Serum anti-collagen IgG, IgM and C-reactive protein (CRP) were analyzed. To understand the inflammation condition of treated animals, production of TNF-α, IL-6 and IL-1β from peritoneal exudates cells (PEC) were also analyzed.P. amboinicussignificantly inhibited the footpad swelling and arthritic symptoms in collagen-induced arthritic rats, while the serum anti-collagen IgM and CRP levels were consistently decreased. The production of pro-inflammatory cytokines TNF-α, IL-6 and IL-1β were also decreased in the high dosage ofP. amboinicusgroup. Here, we demonstrate the potential anti-arthritic effect ofP. amboinicusfor treating RA, which might confer its anti-rheumatic activity. This differs the pharmacological action mode of indomethacin.

Rheumatoid arthritis and p53: how oxidative stress might alter the course of inflammatory diseases

2000 ◽  
Vol 21 (2) ◽  
pp. 78-82 ◽  
Author(s):  
Paul P. Tak ◽  
Nathan J. Zvaifler ◽  
Douglas R. Green ◽  
Gary S. Firestein
Keyword(s):  
Rheumatoid Arthritis ◽  
Oxidative Stress ◽  
Inflammatory Diseases

scholarly journals Dietary fiber intake, the gut microbiome, and chronic systemic inflammation in a cohort of adult men

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Wenjie Ma ◽  
Long H. Nguyen ◽  
Mingyang Song ◽  
Dong D. Wang ◽  
Eric A. Franzosa ◽  
...  
Keyword(s):  
Dietary Fiber ◽  
Systemic Inflammation ◽  
Gut Microbiome ◽  
Inflammatory Diseases ◽  
Fiber Intake ◽  
Carbohydrate Utilization ◽  
Microbiome Composition ◽  
Reactive Protein ◽  
Dietary Fiber Intake

Abstract Background A higher intake of dietary fiber is associated with a decreased risk of chronic inflammatory diseases such as cardiovascular disease and inflammatory bowel disease. This may function in part due to abrogation of chronic systemic inflammation induced by factors such as dysbiotic gut communities. Data regarding the detailed influences of long-term and recent intake of differing dietary fiber sources on the human gut microbiome are lacking. Methods In a cohort of 307 generally healthy men, we examined gut microbiomes, profiled by shotgun metagenomic and metatranscriptomic sequencing, and long-term and recent dietary fiber intake in relation to plasma levels of C-reactive protein (CRP), an established biomarker for chronic inflammation. Data were analyzed using multivariate linear mixed models. Results We found that inflammation-associated gut microbial configurations corresponded with higher CRP levels. A greater intake of dietary fiber was associated with shifts in gut microbiome composition, particularly Clostridiales, and their potential for carbohydrate utilization via polysaccharide degradation. This was particularly true for fruit fiber sources (i.e., pectin). Most striking, fiber intake was associated with significantly greater CRP reduction in individuals without substantial Prevotella copri carriage in the gut, whereas those with P. copri carriage maintained stable CRP levels regardless of fiber intake. Conclusions Our findings offer human evidence supporting a fiber-gut microbiota interaction, as well as a potential specific mechanism by which gut-mediated systemic inflammation may be mitigated.

scholarly journals Relationships of oxidative stress and systemic inflammation markers depending on the degree and duration of hypertension

2016 ◽  
Vol 7 (2) ◽  
pp. 118-122
Author(s):  
T. Ashcheulova ◽  
N. Gerasimchuk
Keyword(s):  
Oxidative Stress ◽  
Arterial Hypertension ◽  
Systemic Inflammation ◽  
Control Group ◽  
C Reactive Protein ◽  
Multisystem Disease ◽  
Reactive Protein ◽  
And Gender ◽  
Relationship Of ◽  
Healthy Persons

Arterial hypertension (AH) is a heterogenic and multisystem disease. It has been suggested that oxidative stress (OS) and systemic non-specific inflammation may be involved in pathogenesis of cardiovascular pathology including AH. The aim of our study was to characterize the plasma C-reactive protein (CRP) level as a marker of systemic inflammation in relation to OS development (on the base of 8-isoprostane level assessment), depending on duration and degree of AH. We examined 117 persons, of which 102 patients from 30 to 65 years old (average age – 54.7 years) who had previously not been receiving regular antihypertensive therapy had I–III degrees of essential hypertension and 15 healthy persons (average age – 48.7 years). In 34 patients from this group the degree of OS activity was determined by 8-isoprostane level as the main marker of OS. The control group consisted of 10 healthy persons, by age and gender comparable with the study group. Determination of plasmatic CRP levels and the level of 8-isoprostane in the serum was performed by ELISA. The study established an increase of the plasmatic CRP levels in patients with hypertension, and a statistically significant increase of serum 8-isoprostane content in hypertensive patients compared to the control group. When assessing the relationship of 8-isoprostane and CRP content in patients with different degrees of hypertension we found that the strongest positive relationship between their levels was observed in the case of I degree hypertension. This may indicate the role of oxidative stress in the pathogenesis of hypertension as a damaging mechanism which contributes to the activation of immune mechanisms and further progression of the disease. Increased CRP and 8-isoprostane levels confirm the involvement of autoimmune mechanisms and oxidative stress in the pathogenesis of hypertension. The level of C-reactive protein is dependent on the duration of hypertension, while the 8-isoprostane levels – only on degree of hypertension. A raised level of C-reactive protein can be used as an independent marker of systemic inflammation in patients with arterial hypertension.

scholarly journals Potential mechanisms of action of celastrol against rheumatoid arthritis: transcriptomic and proteomic analysis

2020 ◽  
Author(s):  
Xinqiang Song ◽  
SONG Xinqiang ◽  
DAI Erqin ◽  
ZHANG Yu ◽  
DU Hongtao ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Oxidative Stress ◽  
Extracellular Matrix ◽  
Quantitative Proteomics ◽  
Inflammatory Diseases ◽  
Mechanisms Of Action ◽  
Label Free ◽  
Expression Of Genes ◽  
Differential Expression Of Genes ◽  
Fibroblast Like Synoviocytes

Abstract Background: The natural triterpene celastrol exhibits potential anti-inflammatory activity in inflammatory diseases such as rheumatoid arthritis (RA). Methods: Here we explored through what proteins and processes celastrol may act in activated fibroblast-like synoviocytes (FLS) from RA patients. Differential expression of genes and proteins after celastrol treatment of FLS was examined using RNA sequencing, label-free relatively quantitative proteomics and molecular docking. Results: Expression of 26,565 genes and 3,372 proteins was analyzed. Celastrol was associated with significant changes in genes that respond to oxidative stress and oxygen levels, as well as genes that stabilize or synthesize components of the extracellular matrix. Conclusions: These results identify several potential mechanisms through which celastrol may inhibit inflammation in RA.

scholarly journals Potential mechanisms of action of celastrol against rheumatoid arthritis: transcriptomic and proteomic analysis

2020 ◽  
Author(s):  
Xinqiang Song ◽  
Erqin Dai ◽  
Yu Zhang ◽  
Hongtao Du ◽  
Lei Wang ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Oxidative Stress ◽  
Extracellular Matrix ◽  
Quantitative Proteomics ◽  
Inflammatory Diseases ◽  
Mechanisms Of Action ◽  
Label Free ◽  
Expression Of Genes ◽  
Differential Expression Of Genes ◽  
Fibroblast Like Synoviocytes

AbstractBackgroundThe natural triterpene celastrol exhibits potential anti-inflammatory activity in inflammatory diseases such as rheumatoid arthritis (RA).MethodsHere we explored through what proteins and processes celastrol may act in activated fibroblast-like synoviocytes (FLS) from RA patients. Differential expression of genes and proteins after celastrol treatment of FLS was examined using RNA sequencing, label-free relatively quantitative proteomics and molecular docking.ResultsExpression of 26,565 genes and 3,372 proteins was analyzed. Celastrol was associated with significant changes in genes that respond to oxidative stress and oxygen levels, as well as genes that stabilize or synthesize components of the extracellular matrix.ConclusionsThese results identify several potential mechanisms through which celastrol may inhibit inflammation in RA.

scholarly journals Vitamin D Deficiency: Effects on Oxidative Stress, Epigenetics, Gene Regulation, and Aging

Biology ◽  
2019 ◽  
Vol 8 (2) ◽  
pp. 30 ◽  
Author(s):  
Sunil J. Wimalawansa
Keyword(s):  
Oxidative Stress ◽  
Vitamin D ◽  
Systemic Inflammation ◽  
Aging Process ◽  
Inflammatory Diseases ◽  
Cost Effective ◽  
Hypovitaminosis D ◽  
Beneficial Effects ◽  
Age Related ◽  
Mitochondrial Functions

Recent advances in vitamin D research indicate that this vitamin, a secosteroid hormone, has beneficial effects on several body systems other than the musculoskeletal system. Both 25 dihydroxy vitamin D [25(OH)2D] and its active hormonal form, 1,25-dihydroxyvitamin D [1,25(OH)2D] are essential for human physiological functions, including damping down inflammation and the excessive intracellular oxidative stresses. Vitamin D is one of the key controllers of systemic inflammation, oxidative stress and mitochondrial respiratory function, and thus, the aging process in humans. In turn, molecular and cellular actions form 1,25(OH)2D slow down oxidative stress, cell and tissue damage, and the aging process. On the other hand, hypovitaminosis D impairs mitochondrial functions, and enhances oxidative stress and systemic inflammation. The interaction of 1,25(OH)2D with its intracellular receptors modulates vitamin D–dependent gene transcription and activation of vitamin D-responsive elements, which triggers multiple second messenger systems. Thus, it is not surprising that hypovitaminosis D increases the incidence and severity of several age-related common diseases, such as metabolic disorders that are linked to oxidative stress. These include obesity, insulin resistance, type 2 diabetes, hypertension, pregnancy complications, memory disorders, osteoporosis, autoimmune diseases, certain cancers, and systemic inflammatory diseases. Vitamin D adequacy leads to less oxidative stress and improves mitochondrial and endocrine functions, reducing the risks of disorders, such as autoimmunity, infections, metabolic derangements, and impairment of DNA repair; all of this aids a healthy, graceful aging process. Vitamin D is also a potent anti-oxidant that facilitates balanced mitochondrial activities, preventing oxidative stress-related protein oxidation, lipid peroxidation, and DNA damage. New understandings of vitamin D-related advances in metabolomics, transcriptomics, epigenetics, in relation to its ability to control oxidative stress in conjunction with micronutrients, vitamins, and antioxidants, following normalization of serum 25(OH)D and tissue 1,25(OH)2D concentrations, likely to promise cost-effective better clinical outcomes in humans.

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