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Please use this identifier to cite or link to this item: http://hdl.handle.net/1942/2708

Title: Cultured astrocytes react to LPS with increased cyclooxygenase activity and phagocytosis
Authors: Kalmar, B.
Kittel, A.
Lemmens, Raf
Kornyei, Z.
Madarasz, E.
Issue Date: 2001
Citation: NEUROCHEMISTRY INTERNATIONAL, 38(5). p. 453-461
Abstract: Phagocytosis and prostaglandin E-2 production were investigated in purified cultures of perinatal rat forebrain astrocytes. Light and electron microscopic data indicated that astrocytes respond to bacterial endotoxin, lipopolysaccharide (LPS) by increased phagocytosis and by activating the cyclooxygenase enzyme-pathway. LPS-inducible phagocytosis of astrocytes was demonstrated by electron microscopic studies on colloidal gold uptake and by photometric determination of fluorescent bead ingestion. The internalisation of fragments of the plasma membrane was shown by histochemical detection of membrane-bound ecto-ATPase activity within intracellular vesicles. Activation of the cyclooxygenase pathway, a characteristic reaction of immune cells under inflammatory conditions, was also detected in astroglial cells upon treatment with LPS. The increased prostaglandin E-2 (PGE(2)) production by astrocytes in response to LPS was reduced by the non-steroid anti-inflammatory drug, indomethacin. Our data indicate that astrocytes display some tissue-protective reactions in response to inflammation inducing factors, even in the absence of peripheral immune cells or central microglia. The role of inducible astrocytic phagocytosis in a non-immune protection-pathway is discussed. (C) 2001 Elsevier Science Ltd. All rights reserved.
Notes: Hungarian Acad Sci, Inst Expt Med, H-1083 Budapest, Hungary. Gedeon Richter Ltd Chem Works, Dept Electrophysiol & Cellular Biol, H-1475 Budapest, Hungary. Limburgs Univ Ctr, MBW Dept, B-3590 Diepenbeek, Belgium.Madarasz, E, Hungarian Acad Sci, Inst Expt Med, Szigony U 43, H-1083 Budapest, Hungary.
URI: http://hdl.handle.net/1942/2708
DOI: 10.1016/S0197-0186(00)00090-5
ISI #: 000167534100011
ISSN: 0197-0186
Category: A1
Type: Journal Contribution
Validation: ecoom, 2002
Appears in Collections: Research publications

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