Escherichia coli–derived and Staphylococcus aureus–derived extracellular vesicles induce MUC5AC expression via extracellular signal related kinase 1/2 and p38 mitogen‐activated protein kinase in human airway epithelial cells

Background Escherichia coli (E. coli) and Staphylococcus aureus (S. aureus) release extracellular vesicles (EVs). E. coli–derived and S. aureus–derived EVs are associated with neutrophilic respiratory inflammation. In neutrophilic respiratory inflammation of human, expression of mucin is increased in airway epithelial cells and is associated with increased morbidity and mortality of the affected patients. However, no study on the effects of EVs on expression of mucin genes has been reported in airway epithelial cells. Therefore, this study was conducted in order to examine the effects and the brief signaling pathways of E. coli–derived and S. aureus–derived EVs on MUC5AC expression in human airway epithelial cells. Methods In mucin‐producing human NCI‐H292 airway epithelial cells and primary cultures of normal nasal epithelial cells, the effects and signaling pathways of E. coli–derived and S. aureus–derived EVs on MUC5AC expression were examined using reverse transcription–polymerase chain reaction (RT‐PCR), real‐time PCR, enzyme immunoassay, and immunoblot analysis with several specific inhibitors and small interfering RNA (siRNA). Results E. coli–derived and S. aureus–derived EVs induced MUC5AC expression. E. coli–derived and S. aureus–derived EVs significantly activated phosphorylation of extracellular signal related kinase 1/2 (ERK1/2) mitogen‐activated protein kinase (MAPK) and p38 MAPK. ERK1/2 MAPK inhibitor, p38 MAPK inhibitor, ERK1/2 MAPK siRNA, and p38 MAPK siRNA significantly blocked E. coli–derived and S. aureus–derived EVs induced MUC5AC messenger RNA (mRNA) expression. Conclusion The results of this study suggest that E. coli–derived and S. aureus–derived EVs induced MUC5AC expression via ERK1/2 and p38 MAPK signaling pathways in human airway epithelial cells.