Mucoid Pseudomonas aeruginosa caused by mucA mutations result in activation of TLR2 in addition to TLR5 in airway epithelial cells
| Autor: | Simon Rousseau, Shantelle L. LaFayette, Trevor Beaudoin, Dao Nguyen |
|---|---|
| Rok vydání: | 2012 |
| Předmět: |
MAPK/ERK pathway
congenital hereditary and neonatal diseases and abnormalities Cystic Fibrosis Biophysics Inflammation Respiratory Mucosa Biology medicine.disease_cause Biochemistry Cystic fibrosis p38 Mitogen-Activated Protein Kinases Microbiology Cell Line fluids and secretions Bacterial Proteins medicine Humans Molecular Biology Pseudomonas aeruginosa Epithelial Cells Cell Biology medicine.disease Phenotype digestive system diseases Toll-Like Receptor 2 respiratory tract diseases TLR2 Toll-Like Receptor 5 TLR5 Cell culture Mutation medicine.symptom |
| Zdroj: | Biochemical and biophysical research communications. 428(1) |
| ISSN: | 1090-2104 |
| Popis: | The presence of the mucoid phenotype of Pseudomonas aeruginosa is a marker of poor survival in cystic fibrosis. As CF lung disease results from chronic infection leading to airway inflammation, we determined whether the switch to a mucoid phenotype by P. aeruginosa has an impact on the inflammatory response of airway epithelial cells. Exposure of airway epithelial cells to non-mucoid and mucoid P. aeruginosa-derived material leads to p38α MAPK activation, a key protein kinase involved in transmitting inflammatory signals. However, while the non-mucoid strain PAO1 activates p38α MAPK pathway solely via TLR5, the mucoid strain PACF508 activates p38α MAPK via both TLR5 and TLR2. Inactivation of mucA (the gene responsible for the mucoid phenotype) in PAO1 leads to p38α MAPK activation by both TLR2 and TLR5, as observed in the clinical mucoid isolate PACF508. Therefore, the switch to mucoid phenotype may contribute to more inflammation via TLR2 activation in addition to TLR5. Our findings highlight an important and under recognized role for TLR2 in the response of airway epithelial cells to infection. |
| Databáze: | OpenAIRE |
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