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Increased interleukin-8 expression by cigarette smoke extract in endothelial cells
1Department of Pharmacology, Faculty of Medicine, The University of Hong, 1/F Li Shu Fan Building, 5 Sassoon Road, Hong Kong
Environmental Toxicology and Pharmacology
|January 4, 2001
Summary
Cigarette smoke extract (CSE) increases Interleukin-8 (IL-8) release from human endothelial cells. This occurs via activation of protein tyrosine kinase (PTK) and protein kinase A (PKA), contributing to gastric lesions.
Area of Science:
- Gastroenterology
- Cell Biology
- Molecular Biology
Background:
- Cigarette smoking exacerbates alcohol-induced gastric lesions.
- Neutrophil infiltration is a key mechanism in this worsening effect.
- Interleukin-8 (IL-8) is a potent neutrophil chemoattractant, suggesting its involvement.
Purpose of the Study:
- To investigate the role of cigarette smoke extract (CSE) in inducing IL-8 expression in endothelial cells.
- To determine the signaling pathways involved in CSE-induced IL-8 secretion.
Main Methods:
- Exposure of ECV304 endothelial cells to different fractions of CSE.
- Measurement of IL-8 secretion.
- Inhibition of specific signaling pathways using kinase inhibitors (PKC, PTK, PKA).
Main Results:
- CSE fractions (ethanol and chloroform soluble) induced a time- and dose-dependent increase in IL-8 secretion.
- Protein kinase C (PKC) inhibition had no significant effect.
- Protein tyrosine kinase (PTK) and protein kinase A (PKA) inhibitors significantly reduced CSE-induced IL-8 expression.
Conclusions:
- CSE stimulates IL-8 release from human endothelial cells.
- This release is mediated by the activation of PTK and PKA signaling pathways.
- These findings highlight a molecular mechanism linking smoking to enhanced gastric inflammation.
