CCL20 Expression via AKT-ERK1/2-AP1 Pathway in Mycoplasma Pneumoniae Infection: Implications for EMT and Cell Migration.

PURPOSE: Mycoplasma pneumoniae, a clinically significant respiratory pathogen, primarily causes community-acquired pneumonia and contributes to asthma development, with its persistent infection frequently resulting in fibrotic pulmonary changes and structural airway abnormalities. This study investigates the signaling pathways regulating CCL20 expression in THP-1 cells following M. pneumoniae infection and its impact on cell migration and epithelial-mesenchymal transition (EMT). METHODS: THP-1 cells were infected with M. pneumoniae, and the expression of CCL20 was measured over time and at various doses. In addition, co-culture experiments were performed using M. pneumoniae-infected THP-1 cells and bronchial epithelial cells to assess EMT and cell migration. RESULTS: M. pneumoniae infection significantly upregulated CCL20 production in THP-1 cells via the AKT-ERK1/2-AP1 pathway, a process that was both time- and dose-dependent. Furthermore, co-culturing M. pneumoniae-infected THP-1 cells with 16HBE cells promoted EMT and increased cell migration, a process that is believed to be associated with CCL20. CONCLUSION: This study provides insights into the molecular mechanisms linking CCL20 to cell migration, highlighting potential therapeutic targets for M. pneumoniae-related lung diseases.