Interleukin-8 (IL-8) in synovial fluid of rheumatoid and nonrheumatoid joint effusions

Verburgh, Cornelis A.; Hart, Mia van der; Aarden, L. A.; Swaak, A. J. G.

doi:10.1007/bf02231778

Cited by 29 publications

(9 citation statements)

References 31 publications

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“…A possible pathogenic role for IL-8 in RA has been suggested by Stricter et al [14] as experiments with neutralising antibodies to IL-8 result in a 27-57% reduction in neutrophil chemotactic bioactivity in RA synovial fluids. In accordance with others [12,15], we found an increased IL-8 level in RA synovial fluid, whereas in our study serum IL-8 was comparable between controls and patients. We did not find a relation between the IL-8 concentration in the synovial fluid and clinical or biological inflammatory parameters.…”

Section: Discussionsupporting

confidence: 82%

Relationship between interleukin-8 and neutrophil adhesion molecules in rheumatoid arthritis

et al. 1996

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To evaluate the role of interleukin-8 (IL-8) on the activation of neutrophils in rheumatoid arthritis (RA), we measured IL-8 and the adhesion molecules, L-selectin (CD62L), CD1 1b and CD18, on neutrophils in paired peripheral blood and synovial fluid of RA patients. Synovial fluid IL-8 levels were significantly increased compared to peripheral blood. L-selectin was split off and CD1 1b and CD 18 were upregulated on neutrophils in the synovial fluid. A positive correlation occurred between the IL-8 concentration and CD18 or CD1 1b densities on neutrophils in the synovial fluid (r = 0.75, P < 0.005 and r = 0.60, P < 0.05, respectively). Peripheral blood neutrophils of the patients were desensitised with IL-8 in vivo, as shown by the significantly lower L-selectin shedding after in vitro IL-8 stimulation: 1.6 times decrease for patients vs 3.2 for controls (P < 0.05). In conclusion, these results add further evidence for the role of IL-8 in the activation of neutrophils in RA.

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Section: Discussionsupporting

confidence: 82%

Relationship between interleukin-8 and neutrophil adhesion molecules in rheumatoid arthritis

et al. 1996

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“…5A). As one of the major chemokines produced by synovial stromal cells, IL-8 plays an important role in attracting neutrophils and peripheral blood monocytes into the inflamed synovium (22,40,59,60), again suggesting a potential link between DEK secretion and inflammatory joint disease.…”

Section: Vol 26 2006 Dek Is a Secreted Chemotactic Factor 9489mentioning

confidence: 99%

The DEK Nuclear Autoantigen Is a Secreted Chemotactic Factor

Mor‐Vaknin

Punturieri

Sitwala

et al. 2006

Molecular and Cellular Biology

134

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The nuclear DNA-binding protein DEK is an autoantigen that has been implicated in the regulation of transcription, chromatin architecture, and mRNA processing. We demonstrate here that DEK is actively secreted by macrophages and is also found in synovial fluid samples from patients with juvenile arthritis. Secretion of DEK is modulated by casein kinase 2, stimulated by interleukin-8, and inhibited by dexamethasone and cyclosporine A, consistent with a role as a proinflammatory molecule. DEK is secreted in both a free form and in exosomes, vesicular structures in which transcription-modulating factors such as DEK have not previously been found. Furthermore, DEK functions as a chemotactic factor, attracting neutrophils, CD8؉ T lymphocytes, and natural killer cells. Therefore, the DEK autoantigen, previously described as a strictly nuclear protein, is secreted and can act as an extracellular chemoattractant, suggesting a direct role for DEK in inflammation.DEK is a mammalian oncoprotein and putative autoantigen whose primary biological function has not been previously elucidated, despite literature linking it to the regulation of transcription, chromatin architecture, and mRNA processing (1,2,11,15,16,24,35,51,65). The DEK protein is widely conserved among species and is transcribed at high levels, especially in hematopoietically derived cells (14,(62)(63)(64). DEK was first characterized as part of the protein product of the DEK-CAN fusion oncogene, resulting from a t(6;9) translocation found in a subset of patients with acute myelogenous leukemia (64). DEK is overexpressed in several different malignancies, including melanoma, hepatocellular carcinoma, glioblastoma, retinoblastoma, bladder cancer, T-cell large granular lymphocyte leukemia, and acute myelogenous leukemia independent of the t(6;9) translocation (7,10,19,20,29,30,32,39,64). Although DEK has previously been described as a strictly nuclear protein, DEK autoreactivity has been identified as a major component of the autoantibody profile in patients with juvenile idiopathic arthritis (JIA) and is also seen in patients with other autoimmune diseases (8,21,38,49,54,55). In the studies presented in this paper, we show that the nuclear protein DEK can be actively secreted by inflammatory cells, is found in synovial fluid samples from JIA patients, and can function as a chemoattractant for inflammatory cells, suggesting a potential role for DEK in immunity and/or autoimmunity. MATERIALS AND METHODSCell preparation. Monocyte-derived macrophages (MDM) were prepared as previously described (31). Briefly, heparinized venous blood samples were collected from healthy volunteers following a protocol approved by the institutional review board, and peripheral blood mononuclear cells were separated by FicollHypaque (Amersham Pharmacia Biotech AB, Uppsala, Sweden) density gradient centrifugation. MDM were purified by adherence to plastic for 2 h at 37°C at a concentration of 5 ϫ 10 5 /ml. Adherent cells were consistently Ͼ90% monocytes (31). Adherence-purified human mon...

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“…Normal values were at less than 20 pg/ml. 15 C-reactive protein (CRP) levels were measured by a sandwich ELISA, using polyclonal rabbit anti-human CRP Abs as catching Abs and biotinylated mAb anti-CRP (CLB anti-CRP-2) as a detecting Ab. Results were referred to a standard (Behringwerke AG, Marburg, Germany) and expressed as milligrams per liter.…”

Section: Assays For Cytokine and Acute Phase Protein Analysismentioning

confidence: 99%

Systemic Toxicity and Cytokine/Acute Phase Protein Levels in Patients After Isolated Limb Perfusion With Tumor Necrosis Factor-a Complicated by High Leakage

et al. 2000

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High leakage of TNFalpha to the systemic circulation, caused by a complicated ILP, led to 10-fold to more than 100-fold increased levels of TNFalpha, IL-6, and IL-8 in comparison with patients without leakage. The increase of the acute phase proteins was limited. Even when high leakage occurs, this procedure should not lead to fatal complications. The most prominent clinical toxicity was hypotension (grade III in four patients), which was easily corrected. No pulmonary or renal toxicity was observed in any patient. It is our experience that, even in the rare event of significant leakage during a TNFa-based ILP, postoperative toxicity is usually mild and can be easily managed by the use of fluid and, in some cases, vasopressors.

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Interleukin-8 (IL-8) in synovial fluid of rheumatoid and nonrheumatoid joint effusions

Cited by 29 publications

References 31 publications

Relationship between interleukin-8 and neutrophil adhesion molecules in rheumatoid arthritis

Relationship between interleukin-8 and neutrophil adhesion molecules in rheumatoid arthritis

The DEK Nuclear Autoantigen Is a Secreted Chemotactic Factor

Systemic Toxicity and Cytokine/Acute Phase Protein Levels in Patients After Isolated Limb Perfusion With Tumor Necrosis Factor-a Complicated by High Leakage

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