IL-1beta induces alkaline phosphatase in human phagocytes
| Autor: | Stavros Frydas, Jacopo Vecchiet, Vincenzo Salini, L.N. Shanmugham, Katia Falasca, Isaia Symeonidou, Stefano Tetè, Pio Conti, Maria Luisa Castellani, Claudia Petrarca |
|---|---|
| Rok vydání: | 2006 |
| Předmět: |
Lipopolysaccharides
Phagocytes Lipopolysaccharide medicine.drug_class Neutrophils Interleukin-1beta General Medicine Receptor antagonist Alkaline Phosphatase Peripheral blood mononuclear cell Molecular biology Monocytes Up-Regulation chemistry.chemical_compound Interleukin 1 Receptor Antagonist Protein chemistry Biochemistry Blood plasma medicine Alkaline phosphatase Humans Arachidonic acid Centrifugation Na+/K+-ATPase |
| Zdroj: | Archives of medical research. 38(1) |
| ISSN: | 0188-4409 |
| Popis: | Background Alkaline phosphatase (ALPase) is found in blood plasma or serum and leukocytes and regulates intercellular processes, maintaining phosphoryl metabolites in a steady state, as well as synthesizing and hydrolyzing phosphate esters on membranes. ALPase supervises the active transport of inorganic phosphates, fats, proteins, carbohydrates and the sodium/potassium pump mechanisms. The formed elements of blood such as polymorphonuclear (PMNs) leucocytes, macrophages (MP) and some lymphocytes are high in ALPase concentrations. Methods In this study we have tested whether the interleukin-1 receptor antagonist (IL-lra) could influence ALPase generation in IL-1β or lipopolysaccharide (LPS)-stimulated neutrophils and MP. Human neutrophils were isolated from heparin-anticoagulated blood drawn from healthy individuals by centrifugation in a two-step gradient, Ficoll-Hypaque. ALPase activity was assessed spectrophotometrically in test tubes containing isolated neutrophils and adherence PBMCs treated with LPS, IL-1β and IL-1ra, alone or in combination. Results IL-lβ or LPS enhanced ALPase in both PMNs and MP, whereas IL-1ra could not inhibit ALPase activity. We performed time course experiments at 0 min, 5 min, 1 h, 24 h, and 43 h (LPS 20 μg/mL, IL-1β 10 ng/mL). No significant increase in ALPase activity was seen until 1 h; however, there was a rapid rise over the next few hours. In another set of experiments using IL-1ra (500 ng/mL), there was no difference between treated cells and control cells. The combination of IL-1β plus IL-1ra did not reduce the ability of IL-1β to induce ALPase activity. Conclusions These data suggest that IL-1β stimulates ALPase through other mechanisms than the release of arachidonic acid products, which are inhibited by IL-lra. |
| Databáze: | OpenAIRE |
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