Galectin-3 inhibits the chemotaxis of human polymorphonuclear neutrophils in vitro

• Verfasst von: Baseras, Billur [VerfasserIn]
• Verfasst von: Gaida, Matthias [VerfasserIn]
• Verfasst von: Kahle, Nadine [VerfasserIn]
• Verfasst von: Schuppel, Ann-Kathrin [VerfasserIn]
• Verfasst von: Kathrey, Diana [VerfasserIn]
• Verfasst von: Prior, Birgit [VerfasserIn]
• Verfasst von: Wente, Moritz N. [VerfasserIn]
• Verfasst von: Hänsch, Gertrud Maria [VerfasserIn]
• Titel: Galectin-3 inhibits the chemotaxis of human polymorphonuclear neutrophils in vitro
• Verf.angabe: Billur Baseras, Matthias M. Gaida, Nadine Kahle, Ann-Kathrin Schuppel, Diana Kathrey, Birgit Prior, Moritz Wente, Gertrud Maria Hänsch
• Jahr: 2012
• Umfang: 8 S.
• Fussnoten: Available online 5 August 2011 ; Gesehen am 24.10.2018
• Titel Quelle: Enthalten in: Immunobiology
• Ort Quelle: München : Elsevier, 1979
• Jahr Quelle: 2012
• Band/Heft Quelle: 217(2012), 1, Seite 83-90
• ISSN Quelle: 1878-3279
• DOI: doi:10.1016/j.imbio.2011.07.031
• Datenträger: Online-Ressource
• Sprache: eng
• K10plus-PPN: 1582236739

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.