Pseudomonas aeruginosa elastase stimulates ERK signaling pathway and enhances IL- 8 production by alveolar epithelial cells in culture
Autor: | Ali Azghani, J. W. Baker, E. J. Miller, Sreerama Shetty, G. J. Bhat |
---|---|
Rok vydání: | 2002 |
Předmět: |
MAPK/ERK pathway
Cell signaling Blotting Western Immunology Biology Cell Line Animals Humans Interleukin 8 Phosphorylation Kinase activity Pancreatic elastase Cells Cultured Pharmacology Pancreatic Elastase Interleukin-8 Epithelial Cells Stimulation Chemical Cell biology Enzyme Activation Pulmonary Alveoli Cell culture Pseudomonas aeruginosa Electrophoresis Polyacrylamide Gel Rabbits Mitogen-Activated Protein Kinases Protein Tyrosine Phosphatases Signal transduction Signal Transduction |
Zdroj: | Inflammation Research. 51:506-510 |
ISSN: | 1420-908X 1023-3830 |
DOI: | 10.1007/pl00012420 |
Popis: | Objective and design: Bacterial products as well as the host airway inflammatory responses contribute to the pathogenesis of Pseudomonas infections. We sought to determine if Pseudomonas elastase (PE) induces mitogen-activated protein (MAP) kinase activity in association with interleukin-8 (IL-8) production by alveolar epithelial cells.¶Methods: We utilized Western blot analysis to detect phosphorylation of signaling intermediates and ELISA was used to measure IL-8 production.¶Results: We found that PE induces phosphorylation of the extracellular signal-regulated (ERK1/2) proteins of the MAPK pathway in A549 epithelial cells. Similar results were obtained using primary cultures of rabbit alveolar type II epithelial cells. PE also enhanced IL-8 production, which was abolished in the presence of the ERK activation inhibitor U0126.¶Conclusions: We conclude that PE activates the ERK1/2 arm of the MAPK pathway and that activation of this pathway results in enhanced IL-8 production. The results demonstrate that PE may augment pulmonary inflammation via cellular signaling that regulates expression of IL-8. |
Databáze: | OpenAIRE |
Externí odkaz: |