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Göteborgs universitets publikationer

IL-17-induced cytokine release in human bronchial epithelial cells in vitro: role of mitogen-activated protein (MAP) kinases

Författare och institution:
Martti Laan (Institutionen för invärtesmedicin, Avdelningen för lungmedicin och allergologi); Jan Lötvall (Institutionen för invärtesmedicin, Avdelningen för lungmedicin och allergologi); K. F. Chung (-); Anders Lindén (Institutionen för invärtesmedicin, Avdelningen för lungmedicin och allergologi)
Publicerad i:
British journal of pharmacology, 133 ( 1 ) s. 200-6
0007-1188 (Print)
Artikel, refereegranskad vetenskaplig
Sammanfattning (abstract):
1. Recent data indicate that interleukin (IL)-17 may contribute to neutrophilic airway inflammation by inducing the release of neutrophil-mobilizing cytokines from airway cells. The aim of this study was to evaluate the role of mitogen activated protein kinases in IL-17 induced release of IL-8 and IL-6 in bronchial epithelial cells. 2. Transformed human bronchial epithelial cells (16HBE) were stimulated with either IL-17 or vehicle. Both groups were treated either with SB202190 (inhibitor of p38 MAP kinase), PD98059 (inhibitor of extracellular-signal-regulated kinase [ERK] pathway), Ro-31-7549 (protein kinase C [PKC] inhibitor), LY 294002 (a phosphatidylinositol 3-kinase [PI 3-kinase] inhibitor) or vehicle. IL-6 and IL-8 levels were measured in conditioned media by ELISA. 3. The IL-17-induced release of IL-6 and IL-8 was concentration-dependently inhibited by SB202190 and by PD98059 in bronchial epithelial cells without affecting cell proliferation or survival. 4. Ro-31-7549 and LY294002 had no significant effect on IL-17-induced IL-6 or IL-8 release in bronchial epithelial cells. 4. Taken together, these data indicate a role for p38 and ERK kinase pathways in IL-17-induced release of neutrophil-mobilizing cytokines in human bronchial epithelial cells. These mechanisms constitute potential pharmacotherapeutical targets for inhibition of the IL-17-mediated airway neutrophilia.
Ämne (baseras på Högskoleverkets indelning av forskningsämnen):
Klinisk medicin ->
Lungmedicin och allergi
1-Phosphatidylinositol 3-Kinase/antagonists & inhibitors/metabolism, Bronchi/cytology/*drug effects/enzymology/metabolism, Cell Division/drug effects, Cell Line, Transformed, Cytokines/metabolism/*secretion, Enzyme Inhibitors/pharmacology, Epithelial Cells/cytology/*drug effects/enzymology/metabolism, Humans, Interleukin-17/*pharmacology, Interleukin-6/metabolism/secretion, Interleukin-8/metabolism/secretion, MAP Kinase Kinase 1, MAP Kinase Signaling System/drug effects, Mitogen-Activated Protein Kinase Kinases/antagonists &, inhibitors/metabolism, Mitogen-Activated Protein Kinases/antagonists & inhibitors/*metabolism, Protein Kinase C/antagonists & inhibitors/metabolism, Protein-Serine-Threonine Kinases/antagonists & inhibitors/metabolism, p38 Mitogen-Activated Protein Kinases
Postens nummer:
Posten skapad:
2007-09-27 11:19
Posten ändrad:
2011-01-20 09:59

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