Effect of Staphylococcus aureus in pneumonia mouse model on promotion of mBD-3 expression through ERK1/2 pathway

Abstract

Background/Aim. Staphylococcus aureus (S. aureus) is a Gram-positive pathogen that is causing various human diseases. This bacteria causes pneumonia, which is characterized by localized tissue necrosis. The aim of the study was to explore the expression of mouse ?-defensin 3 (mBD-3) induced by S. aureus in mouse lungs and the effect of mBD-3 expression on the mitogen-activated protein kinase (MAPK) pathway. Methods. A S. aureus pneumonia mouse model was developed, and the expression of mBD-3 and the MAPK pathway was investigated by immunofluorescence and western blot. Results. The S. aureus pneumonia mouse model was created successfully. The number of white blood cells was elevated at 48h and 72 h, and bronchiolar mucosal hyperemia was observed, along with a large number of white blood cells and mucus in the bronchioles. The expression levels of mBD-3 at 48h and 72 h were greater than the levels in the control and at 24 h. The amount of phosphorylated ERK1/2 was increased at 48h and 72 h compared with the level in the control and at 24 h. The expression of mBD-3 was lower when ERK1/2 phosphorylation was inhibited by U0126. Conclusion. The S. aureus signaling pathway accelerates mBD-3 expression mainly through an ERK-dependent pathway in the mouse lung.