title: Galectin-3 inhibits the chemotaxis of human polymorphonuclear neutrophils in vitro.
abstract: In the recent years, the participation of the animal lectin galectin (gal)-3 in inflammation and in host defence mechanisms was extensively studied. In vivo studies implied - among others - a role of gal-3 in the recruitment of polymorphonuclear neutrophils (PMN) to sites of bacterial infection. In that context, we asked the question whether gal-3 was chemotactic for PMN. Functional assays revealed that gal-3 was not chemotactic for PMN, but that it inhibited the spontaneous migration and the chemotaxis of PMN towards complement C5a, interleukin (IL)-8, or ATP. Moreover, gal-3 inhibited the shape change and the actin polymerisation of PMN that occurs in response to C5a or IL-8. By use of FITC-labelled gal-3, we found that it attached rapidly to the PMN membrane in a lactose-sensitive manner. In response to gal-3 the MAP kinase p38 was phosphorylated. This kinase is crucial for the migration of PMN towards end-target chemokines, such as C5a, and is activated in response to C5a or IL-8. When PMN were preincubated with gal-3, the C5a-induced p38 phosphorylation was transiently enhanced, but eventually down-modulated. We conclude that by interfering with the chemokine-induced p38 phosphorylation gal-3 inhibits chemotaxis of PMN.
authors: Institut für Immunologie, Germany.
authors: Billur
authors: B
authors: Baseras
authors: Matthias M
authors: MM
authors: Gaida
authors: Nadine
authors: N
authors: Kahle
authors: Ann-Kathrin
authors: AK
authors: Schuppel
authors: Diana
authors: D
authors: Kathrey
authors: Birgit
authors: B
authors: Prior
authors: Moritz
authors: M
authors: Wente
authors: Gertrud Maria
authors: GM
authors: Hänsch
mesh_terms: D000199:Actins / Q000276:immunology / Q000378:metabolism; D000255:Adenosine Triphosphate / Q000276:immunology / Q000378:metabolism; D015153:Blotting, Western; D002478:Cells, Cultured; D002634:Chemotaxis, Leukocyte / Q000187:drug effects* / Q000276:immunology; D015936:Complement C5a / Q000276:immunology* / Q000378:metabolism / Q000494:pharmacology; D005434:Flow Cytometry; D016650:Fluorescein-5-isothiocyanate / Q000032:analysis; D037502:Galectin 3 / Q000276:immunology* / Q000378:metabolism / Q000494:pharmacology; D006801:Humans; D007113:Immunity, Innate; D007249:Inflammation / Q000276:immunology* / Q000378:metabolism; D016209:Interleukin-8 / Q000276:immunology* / Q000378:metabolism / Q000494:pharmacology; D009504:Neutrophils / Q000166:cytology / Q000187:drug effects / Q000276:immunology* / Q000378:metabolism; D010766:Phosphorylation / Q000187:drug effects / Q000276:immunology; D058105:Polymerization; D015398:Signal Transduction / Q000187:drug effects / Q000276:immunology; D048051:p38 Mitogen-Activated Protein Kinases / Q000276:immunology / Q000378:metabolism
chemical_list: D000199:Actins; D037502:Galectin 3; D016209:Interleukin-8; D015936:Complement C5a; D000255:Adenosine Triphosphate; D048051:p38 Mitogen-Activated Protein Kinases; D016650:Fluorescein-5-isothiocyanate