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Your search keyword '"Heeringa P"' showing total 17 results
Start Over Author "Heeringa P" Publisher bmj
17 results on '"Heeringa P"'

2. OP0091 EXPANSION OF MYELOPEROXIDASE (MPO)-SPECIFIC IgM B CELLS IN ANTI-NEUTROPHIL CYTOPLASMIC ANTIBODY (ANCA)-ASSOCIATED VASCULITIS

Author

Wortel, C., primary, van de Wetering, R., additional, van Dooren, H., additional, Stork, E. M., additional, Bakker, A. M., additional, Brehler, A. S., additional, Kissel, T., additional, Reijm, S., additional, Stoeken-Rijsbergen, G., additional, van Schie, K., additional, Rutgers, A., additional, Trouw, L. A., additional, Huizinga, T., additional, Teng, Y. K. O., additional, van Kooten, C., additional, Heeringa, P., additional, Toes, R., additional, and Scherer, H. U., additional

Published
2022
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7. POS0809 A BIOMARKER PROFILE AIDING AN EARLY DIAGNOSIS OF GIANT CELL ARTERITIS

Author

Van Sleen, Y., primary, Therkildsen, P., additional, Boots, A., additional, Dalsgaard Nielsen, B., additional, Van der Geest, K., additional, Heeringa, P., additional, Huitema, M. G., additional, Posthumus, M. D., additional, Sandovici, M., additional, Toonen, E., additional, Zijlstra, J., additional, Hauge, E. M., additional, and Brouwer, E., additional

Published
2021
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14. Effects of p38 mitogen-activated protein kinase inhibition on anti-neutrophil cytoplasmic autoantibody pathogenicity in vitro and in vivo

Author

van der Veen, B. S., primary, Chen, M., additional, Muller, R., additional, van Timmeren, M. M., additional, Petersen, A. H., additional, Lee, P. A., additional, Satchell, S. C., additional, Mathieson, P. W., additional, Saleem, M. A., additional, Stegeman, C. A., additional, Zwerina, J., additional, Molema, G., additional, and Heeringa, P., additional

Published
2010
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16. Expression of interleukin-6 in synovial tissue of patients with polymyalgia rheumatica.

Author

Jiemy WF, Zhang A, Boots AMH, Heeringa P, Sandovici M, Diepstra A, Hein S, Dasgupta B, Brouwer E, and van der Geest KS

Subjects
Humans, Interleukin-6, Synovial Membrane metabolism, Polymyalgia Rheumatica, Giant Cell Arteritis
Abstract

Competing Interests: Competing interests: KSMvdG reports personal fees from Roche, outside the submitted work. BD reports consulting fees from Roche, Chugai, Sanofi, and sponsorship grants for international meetings and workshops with Roche, Sanofi, AbbVie and GlaxoSmithKline. EB reports personal fees from Roche, outside the submitted work. The other authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Published
2023
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17. Effects of p38 mitogen-activated protein kinase inhibition on anti-neutrophil cytoplasmic autoantibody pathogenicity in vitro and in vivo.

Author

van der Veen BS, Chen M, Müller R, van Timmeren MM, Petersen AH, Lee PA, Satchell SC, Mathieson PW, Saleem MA, Stegeman CA, Zwerina J, Molema G, and Heeringa P

Subjects
Animals, Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis enzymology, Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis immunology, Cells, Cultured, Cytokines biosynthesis, Disease Models, Animal, Drug Evaluation, Preclinical methods, Female, Glomerulonephritis enzymology, Glomerulonephritis immunology, Glomerulonephritis prevention & control, Humans, Immunoglobulin G immunology, Kidney Glomerulus immunology, Lipopolysaccharides immunology, MAP Kinase Signaling System physiology, Mice, Mice, Knockout, Neutrophil Activation immunology, Peroxidase immunology, Protein Kinase Inhibitors therapeutic use, Respiratory Burst immunology, p38 Mitogen-Activated Protein Kinases physiology, Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis prevention & control, Antibodies, Antineutrophil Cytoplasmic immunology, Protein Kinase Inhibitors pharmacology, p38 Mitogen-Activated Protein Kinases antagonists & inhibitors
Abstract

Objective: To determine whether inhibition of p38 mitogen-activated protein kinase (p38MAPK) reduces the pathogenicity of anti-neutrophil cytoplasmic autoantibodies (ANCAs) in vitro and in vivo., Methods: The effects of the p38MAPK-specific inhibitor AR-447 were studied in vitro using neutrophil respiratory burst and degranulation assays, and in lipopolysaccharide (LPS)-stimulated human glomerular endothelial cells. In vivo, p38MAPK inhibition was investigated in a mouse anti-myeloperoxidase (MPO) IgG/LPS glomerulonephritis model. Mice were treated orally with AR-447 daily, starting before (pretreatment group) or 24 h after disease onset (treatment group), and killed after 1 or 7 day(s)., Results: In vitro, AR-447 diminished neutrophil respiratory burst and degranulation induced by patient-derived MPO-ANCA and proteinase 3 (Pr3)-ANCA. In glomerular endothelial cells, AR-447 reduced LPS-induced secretion of IL-6 and IL-8, but not of MCP-1. In mice, pretreatment with AR-447 reduced albuminuria 1 day after induction of glomerulonephritis. After 7 days, no effects on urinary abnormalities were observed upon AR-447 pretreatment or treatment. Also, glomerular neutrophil accumulation was not diminished. In contrast, glomerular macrophage accumulation and the formation of glomerular crescents was significantly reduced by AR-447 pretreatment (vehicle: 12.5 ± 5.6% crescentic glomeruli; AR-447: 7.7 ± 2.7%) and treatment (vehicle 14.6 ± 1.8%; AR-447 6.0 ± 3.4%) at 7 days., Conclusion: This study shows that p38MAPK inhibition markedly reduces ANCA-induced neutrophil activation in vitro. In vivo, p38MAPK inhibition partly reduced crescent formation when the drug was administered prior to disease induction and after disease onset, suggesting that besides p38MAPK activity other signalling pathways contribute to the disease activity.

Published
2011
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