Medizinische Universität Graz Austria/Österreich - Forschungsportal - Medical University of Graz
Gewählte Publikation:
SHR Neuro Krebs Kardio Lipid Stoffw Microb
Koller, H; Hochegger, K; Zlabinger, GJ; Lhotta, K; Mayer, G; Rosenkranz, AR.
Apoptosis of human polymorphonuclear neutrophils accelerated by dialysis membranes via the activation of the complement system.
Nephrol Dial Transplant. 2004; 19(12):3104-3111
Doi: 10.1093/ndt/gfh500
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- Führende Autor*innen der Med Uni Graz
- Rosenkranz Alexander
- Co-Autor*innen der Med Uni Graz
- Eller Kathrin
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- Abstract:
- Background. Haemodialysis (HD) with bioincompatible cellulosic membranes like Cuprophan (CU) is considered to influence negatively the clinical outcome of acute and chronic renal failure. In this effect, apart from the disturbance of phagocytosis or oxygen species production by leukocytes, increased apoptosis also has been implicated recently. The objective of this study was to study the effect of HD membranes on apoptosis induction in polymorphonuclear neutrophils (PMN). Methods. PMN from healthy donors and uraemic patients were isolated and apoptosis was induced by co-incubation with CU, Hemophan or polyamide hollow fibres in the presence of serum from healthy or uraemic humans. Apoptosis was quantified by flow cytometry using Annexin V-FITC and propidium iodide staining and was confirmed by the detection of DNA fragmentation on gel electrophoresis. The deposition of immunoglobulins (Ig) and complement factors on hollow fibres was detected by direct immunofluorescence. Results. Heat inactivation or the depletion of complement components or Ig significantly reduced apoptosis, indicating its dependence on classical complement activation. The detection of IgG on hollow CU fibres and the restored acceleration of apoptosis by the appropriate replenishment of Ig-deficient sera additionally confirmed these findings. Inhibition experiments revealed that caspases were necessary mainly, but not exclusively, for apoptosis to occur after complement activation. Uraemia led to increased PMN apoptosis in the presence of bioincompatible, but not biocompatible, membranes. Conclusions. Our results suggest that the acceleration of PMN apoptosis in the presence of CU is mediated via an antibody-dependent activation of the classical complement pathway mobilizing both caspase-dependent and -independent pathways.
- Find related publications in this database (using NLM MeSH Indexing)
- Apoptosis - physiology
- Biocompatible Materials -
- Complement Activation - physiology
- Complement System Proteins - metabolism
- Humans -
- Kidney Failure, Chronic - blood Kidney Failure, Chronic - therapy
- Membranes, Artificial -
- Neutrophils - cytology Neutrophils - pathology Neutrophils - physiology
- Reference Values -
- Renal Dialysis -
- Uremia - blood Uremia - therapy
- Find related publications in this database (Keywords)
- apoptosis
- biocompatibility
- complement system
- dialysis membranes
- neutrophils