Journal
INFLAMMATION RESEARCH
Volume 51, Issue 10, Pages 506-510Publisher
SPRINGER BASEL AG
DOI: 10.1007/PL00012420
Keywords
Pseudomonas elastase; signal transduction; MAPK; cytokines; lung epithelium
Categories
Funding
- NHLBI NIH HHS [LHB1 55622, HL 45018, HL 62453] Funding Source: Medline
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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 ERK 1/2 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.
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