Circulating tumour necrosis factor alpha and soluble tumour necrosis factor receptors in patients with different patterns of rheumatoid synovitis

Klimiuk, Piotr Adrian; Sierakowski, Stanisław; Latosiewicz, Robert; Cylwik, Jacek; Cylwik, B; Skowroński, J; Chwiećko, Justyna

doi:10.1136/ard.62.5.472

Cited by 55 publications

(32 citation statements)

References 10 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Because TNF-␣ is thought to be involved in the progression of diabetic retinopathy and ocular inflammation (15)(16)(17)(18)(19)(20), our finding that TNF-␣ raises the activity of core 2 GlcNAc-T suggests the physiological relevance of O-linked oligosaccharides in the development and/or progression of this pathological condition. In this respect, it is possible that leukocyte-endothelial cell adhesion in the retina is mediated by P-selectin glycoprotein ligand-1, a predominant ligand for selectins, which requires decoration with core 2 branched O-glycans for proper function (48 -50).…”

Section: Diabetes Vol 53 November 2004mentioning

confidence: 79%

Tumor Necrosis Factor-α in Diabetic Plasma Increases the Activity of Core 2 GlcNAc-T and Adherence of Human Leukocytes to Retinal Endothelial Cells

Ben-Mahmud

Mann

Datti³

et al. 2004

Diabetes

View full text Add to dashboard Cite

A large body of evidence now implicates increased leukocyte-endothelial cell adhesion as a key early event in the development of diabetic retinopathy. We recently reported that raised activity of the glycosylating enzyme core 2 ␤ 1,6-N-acetylglucosaminyltransferase (GlcNAc-T) through protein kinase C (PKC)␤2-dependent phosphorylation plays a fundamental role in increased leukocyteendothelial cell adhesion and capillary occlusion in retinopathy. In the present study, we demonstrate that following exposure to plasma from diabetic patients, the human promonocytic cell line U937 exhibits a significant elevation in core 2 GlcNAc-T activity and increased adherence to cultured retinal capillary endothelial cells. These effects of diabetic plasma on enzyme activity and cell adhesion, mediated by PKC␤2-dependent phosphorylation of the core 2 GlcNAc-T protein, were found to be triggered by increased plasma levels of tumor necrosis factor (TNF)-␣. Levels of enzyme activity in plasma-treated U937 cells were closely dependent on the severity of diabetic retinopathy, with the highest values observed upon treatment with plasma of patients affected by proliferative retinopathy. Furthermore, we noted much higher correlation, as compared with control subjects, between increased values of core 2 GlcNAc-T activity and cell adhesion properties. Based on the prominent role of TNF-␣ in the development of diabetic retinopathy, these observations further validate the significance of core 2 GlcNAc-T in the pathogenesis of capillary occlusion, thereby enhancing the therapeutic potential of specific enzyme inhibitors.

show abstract

Section: Diabetes Vol 53 November 2004mentioning

confidence: 79%

Tumor Necrosis Factor-α in Diabetic Plasma Increases the Activity of Core 2 GlcNAc-T and Adherence of Human Leukocytes to Retinal Endothelial Cells

Ben-Mahmud

Mann

Datti³

et al. 2004

Diabetes

View full text Add to dashboard Cite

show abstract

“…Whereas previous work highlighted a possible role for synovial B-cell and plasma cell quantitative infiltration in predicting future diagnosis of RA in early arthritis [49], a very recent report failed to confirm disease-specific diagnostic and prognostic properties of lymphocyte aggregates-evaluated through CD3 + T-cell expression-in arthritis patients with disease duration of less than 12 months [7]. Similarly, variable associations with disease severity in established RA in terms of therapeutic burden and radiographic damage arise from different studies focusing on heterogeneous aspects of the process of lymphocyte aggregation and organization [50][51][52]. Again, depending on how the synovial aggregates are categorized, this may lead to opposite conclusions with regard to their capacity for predicting clinical response to tumor necrosis factor (TNF) inhibitors [52,53].…”

Section: Heterogeneity Of Synovial Patterns Of Cell Infiltrationmentioning

confidence: 93%

Synovial Tissue Heterogeneity and Peripheral Blood Biomarkers

et al. 2011

View full text Add to dashboard Cite

Rheumatoid arthritis is characterized by multiple pathobiological processes and heterogeneous clinical phenotypes. Not surprisingly, the inflamed synovium harbors an equally complex pathology. This includes variability in infiltrating and resident cell populations, spatial arrangements, and cell-cell interactions, as well as gene expression profiles. Remarkable progress in our understanding of the many facets of tissue heterogeneity has been facilitated by the increasing availability of patients' material and the development of advanced research technologies. The next challenge is to capitalize on the large amount of data generated to elucidate the specific pathogenic pathways disparately activated in different patients and/or different phases of the disease. When tissue pathology can be reliably explored through noninvasive circulating biomarkers, then the circle will be closed. We attempt to highlight key advances in the understanding of synovial tissue heterogeneity in rheumatoid arthritis and summarize novel perspectives in synovial biomarker discovery in relation to peripheral blood.

show abstract

“…The exacerbation of synovitis as a result of cell activation by hyperlipidemia has not been reported previously. However, a greater immunologic activation and potential for joint destruction in patients with RA has been associated with a specific pattern of circulating and synovial cytokine concentrations (53)(54)(55)(56).…”

Section: Discussionmentioning

confidence: 99%

Chronic arthritis aggravates vascular lesions in rabbits with atherosclerosis: A novel model of atherosclerosis associated with chronic inflammation

Largo

Sánchez‐Pernaute

Marcos

et al. 2008

Arthritis & Rheumatism

View full text Add to dashboard Cite

Objective. To determine whether systemic inflammation induced by chronic antigen-induced arthritis (AIA) accelerates vascular lesions in rabbits with atherosclerosis.Methods. Two models of atherosclerosis and chronic AIA were combined. Atherosclerosis was induced by coupling a hyperlipemic diet with an endothelial lesion at the femoral arteries, while chronic AIA was induced by ovalbumin injection. Markers in sera and peripheral blood mononuclear cells (PBMCs) as well as vessels and synovial membranes from the rabbits with the double phenotype (both chronic AIA and atherosclerosis) were compared with those from rabbits with each disease alone.Results. Serum levels of interleukin-6, C-reactive protein, and prostaglandin E 2 increased in rabbits with both chronic AIA and atherosclerosis as compared with healthy animals or animals with either chronic AIA alone or atherosclerosis alone. NF-B binding and CCL2 and cyclooxygenase 2 (COX-2) expression were higher in PBMCs from rabbits with both chronic AIA and atherosclerosis than in PBMCs from healthy rabbits. The intima-media thickness ratio of femoral arteries was equally increased in rabbits with atherosclerosis alone and in rabbits with both chronic AIA and atherosclerosis, but the latter group showed a higher level of macrophage infiltration. Femoral CCL2 and COX-2 expression was increased in rabbits with both chronic AIA and atherosclerosis as compared with rabbits with atherosclerosis alone. In the aortas, vascular lesions were found in 27% of rabbits with atherosclerosis alone and in 60% of rabbits with both chronic AIA and atherosclerosis. Rabbits with both chronic AIA and atherosclerosis exhibited more severe synovitis and higher synovial expression of CCL2 than did rabbits with chronic AIA alone.Conclusion. The onset of chronic AIA in animals with atherosclerosis resulted in the local and systemic up-regulation of mediators of tissue inflammation and plaque instability associated with a higher incidence of aortic lesions. This model could represent a novel approach to the study of inflammation-associated atherosclerosis.

show abstract

Circulating tumour necrosis factor alpha and soluble tumour necrosis factor receptors in patients with different patterns of rheumatoid synovitis

Cited by 55 publications

References 10 publications

Tumor Necrosis Factor-α in Diabetic Plasma Increases the Activity of Core 2 GlcNAc-T and Adherence of Human Leukocytes to Retinal Endothelial Cells

Tumor Necrosis Factor-α in Diabetic Plasma Increases the Activity of Core 2 GlcNAc-T and Adherence of Human Leukocytes to Retinal Endothelial Cells

Synovial Tissue Heterogeneity and Peripheral Blood Biomarkers

Chronic arthritis aggravates vascular lesions in rabbits with atherosclerosis: A novel model of atherosclerosis associated with chronic inflammation

Contact Info

Product

Resources

About