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Your search keyword '"Annemarie A. J. H. M. van Bijnen"' showing total 2 results
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2 results on '"Annemarie A. J. H. M. van Bijnen"'

1. Lipocalin-2 and neutrophil activation in pancreatic cancer cachexia

Author

Min Deng, Merel R. Aberle, Annemarie A. J. H. M. van Bijnen, Gregory van der Kroft, Kaatje Lenaerts, Ulf P. Neumann, Georg Wiltberger, Frank G. Schaap, Steven W. M. Olde Damink, and Sander S. Rensen

Subjects
cancer cachexia, neutrophil activation, innate immunity, appetite, lipocalin-2, nutritional status, Immunologic diseases. Allergy, RC581-607
Abstract

BackgroundCancer cachexia is a multifactorial syndrome characterized by body weight loss and systemic inflammation. The characterization of the inflammatory response in patients with cachexia is still limited. Lipocalin-2, a protein abundant in neutrophils, has recently been implicated in appetite suppression in preclinical models of pancreatic cancer cachexia. We hypothesized that lipocalin-2 levels could be associated with neutrophil activation and nutritional status of pancreatic ductal adenocarcinoma (PDAC) patients.MethodsPlasma levels of neutrophil activation markers calprotectin, myeloperoxidase, elastase, and bactericidal/permeability-increasing protein (BPI) were compared between non-cachectic PDAC patients (n=13) and cachectic PDAC patients with high (≥26.9 ng/mL, n=34) or low (

Published
2023
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2. Inhibition of complement factor C5 protects against renal ischemia-reperfusion injury: inhibition of late apoptosis and inflammation

Author

Bart, De Vries, Robert A, Matthijsen, Tim G A M, Wolfs, Annemarie A J H M, Van Bijnen, Peter, Heeringa, and Wim A, Buurman

Subjects
Male, Nephritis, Neutrophils, Antibodies, Monoclonal, Complement C5, Apoptosis, Complement Membrane Attack Complex, Kidney, Blood Urea Nitrogen, Mice, Creatinine, Reperfusion Injury, Animals, Complement Activation
Abstract

Complement has been implicated in the pathophysiology of renal ischemia-reperfusion (I/R) injury. However, the mechanism underlying complement-mediated renal I/R injury is thus far unknown. To investigate the involvement of complement in I/R injury, we studied the activation and deposition of complement in a murine model of renal I/R injury. Furthermore, we examined the effect of inhibition of complement-factor C5 on renal I/R injury.Mice were subjected to 45 min of unilateral ischemia and subsequent contralateral nephrectomy and reperfusion for 2, 12, or 24 hr. Mice were control treated or treated with BB5.1, a monoclonal antibody that prevents cleavage of complement factor C5, thereby preventing C5a generation and formation of the membrane attack complex (MAC).Renal I/R induced extensive deposition of C3 early after reperfusion, whereas C6 and C9 deposition (MAC formation) occurred relatively late. I/R-induced complement deposition was mainly localized to tubular epithelium. Treatment with BB5.1 totally prevented MAC formation but also reduced C3 deposition. Inhibition of C5 strongly inhibited late inflammation, as measured by neutrophil influx and induction of the murine CXC chemokines macrophage inflammatory protein-2, KC, and lipopolysaccharide-induced CXC chemokine. Anti-C5 treatment furthermore abrogated late I/R-induced apoptosis, whereas early apoptosis was not affected. Moreover, BB5.1 treatment significantly protected against I/R-induced renal dysfunction.Renal I/R is followed by activation of the complement system and intrarenal deposition of C3 and MAC. Complement activation plays a crucial role in the regulation of inflammation and late apoptosis. Complement inhibition, by preventing C5 activation, abrogates late apoptosis and inflammation, being strongly protective against renal function loss.

Published
2003

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