Sökning: id:"swepub:oai:gup.ub.gu.se/253932" >
Galectin-3 activate...
Galectin-3 activates the NADPH-oxidase in exudated but not peripheral blood neutrophils.
-
- Karlsson, Anna, 1967 (författare)
- Gothenburg University,Göteborgs universitet,Institutionen för invärtesmedicin, Avdelningen för reumatologi och inflammationsforskning,Institute of Internal Medicine, Dept of Rheumatology and Inflammation Research
-
Follin, P (författare)
-
Leffler, H (författare)
-
visa fler...
-
- Dahlgren, Claes, 1949 (författare)
- Gothenburg University,Göteborgs universitet,Institutionen för invärtesmedicin, Avdelningen för reumatologi och inflammationsforskning,Institutionen för medicinsk mikrobiologi och immunologi,Institute of Internal Medicine, Dept of Rheumatology and Inflammation Research,Institute of Medical Microbiology/Immunology
-
visa färre...
-
(creator_code:org_t)
- 1998
- 1998
- Engelska.
-
Ingår i: Blood. - 0006-4971. ; 91:9, s. 3430-8
- Relaterad länk:
-
https://gup.ub.gu.se...
Abstract
Ämnesord
Stäng
- Galectin-3, a lactose-binding mammalian lectin that is secreted from activated macrophages, basophils, and mast cells, was investigated with respect to its ability to activate the human neutrophil NADPH-oxidase. The galectin-3-induced activity was determined with in vivo exudated cells (obtained from a skin chamber) and compared with that of peripheral blood neutrophils. Galectin-3 was found to be a potent activator of the NADPH-oxidase only in exudated neutrophils and the binding of galectin-3 to the surface of these cells was increased compared with peripheral blood cells. Different in vitro priming protocols resulting in degranulation were used to mimic the exudation process in terms of increasing the receptor exposure on the cell surface. Galectin-3 could induce an oxidative response similar to that in exudated cells only after a significant amount of the intracellular organelles had been mobilized. This increase in oxidative response was paralleled by an increased binding of galectin-3 to the surface of the cells. The major conclusion of the study is that galectin-3 is a potent stimulus of the neutrophil respiratory burst, provided that the cells have first experienced an extravasation process. The results also imply that the neutrophil response to galectin-3 could be mediated through receptors mobilized from intracellular granules, and we report the presence of galectin-3-binding proteins in such organelles.
Ämnesord
- MEDICIN OCH HÄLSOVETENSKAP -- Medicinska och farmaceutiska grundvetenskaper -- Immunologi inom det medicinska området (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Basic Medicine -- Immunology in the medical area (hsv//eng)
Nyckelord
- Alkaline Phosphatase
- metabolism
- Antigens
- Differentiation
- physiology
- Cells
- Cultured
- Enzyme Activation
- Exudates and Transudates
- cytology
- Galectin 3
- Humans
- Macrophage-1 Antigen
- metabolism
- NADPH Oxidase
- metabolism
- Neutrophil Activation
- Neutrophils
- enzymology
- Receptors
- Cell Surface
- metabolism
- Receptors
- Complement 3b
- metabolism
- Respiratory Burst
- drug effects
- Signal Transduction
Publikations- och innehållstyp
- ref (ämneskategori)
- art (ämneskategori)
Hitta via bibliotek
-
Blood
(Sök värdpublikationen i LIBRIS)
Till lärosätets databas