Adenovirus E1A upregulates interleukin-8 expression induced by endotoxin in pulmonary epithelial cells
| Autor: | W M. Elliott, Naoto Keicho, James C. Hogg, Shizu Hayashi |
|---|---|
| Rok vydání: | 1997 |
| Předmět: |
Lipopolysaccharides
Pulmonary and Respiratory Medicine Transcription Genetic Physiology viruses medicine.medical_treatment Inflammation Biology Transfection medicine.disease_cause Epithelium Cell Line Proinflammatory cytokine Physiology (medical) Granulocyte Colony-Stimulating Factor Escherichia coli medicine Humans Macrophage RNA Messenger Interleukin 8 Lung Monocyte Interleukin-8 Granulocyte-Macrophage Colony-Stimulating Factor Interleukin Cell Biology Recombinant Proteins Monocyte Chemoattractant Proteins Endotoxins Adenoviridae medicine.anatomical_structure Cytokine Gene Expression Regulation Immunology Cancer research Cytokines Adenovirus E1A Proteins medicine.symptom DNA Probes |
| Zdroj: | Scopus-Elsevier |
| ISSN: | 1522-1504 1040-0605 |
| DOI: | 10.1152/ajplung.1997.272.6.l1046 |
| Popis: | Adenovirus E1A DNA and proteins are frequently detected in lungs of patients with chronic obstructive pulmonary disease. Because adenovirus E1A can regulate host gene expression by interacting with cellular transcription factors, we postulate that E1A enhances synthesis of inflammatory mediators. To examine this possibility, we measured the expression of inflammatory cytokines in E1A-producing A549 human pulmonary epithelial cells and control cells. Interleukin (IL)-8 mRNA was markedly induced by lipopolysaccharide (LPS) in E1A-producing cells but not in controls. IL-8 protein levels were elevated in parallel. In both cell types, monocyte chemotactic and activating factor mRNA induced by LPS was low, and transforming growth factor-beta 1 mRNA was not affected. IL-1 beta, IL-6, granulocyte macrophage colony-stimulating factor, and granulocyte colony-stimulating factor mRNAs were too low to show any effect of E1A. We conclude that the LPS responsiveness of A549 pulmonary epithelial cells is altered by adenoviral E1A by upregulating IL-8. We speculate that this mechanism may be important in the amplification of the inflammatory process of lungs to other irritants. |
| Databáze: | OpenAIRE |
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