CCL20 Expression via AKT-ERK1/2-AP1 Pathway in Mycoplasma Pneumoniae Infection: Implications for EMT and Cell
Xue Yang1,2, Daoyong Liao1, Ying Huang1
1The Affiliated Nanhua Hospital, Department of Clinical Laboratory, Hengyang Medical School, University of South China, Hengyang, People's Republic of China.
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.
Insights
Mycoplasma pneumoniae infection boosts CCL20 production via the AKT-ERK1/2-AP1 pathway. This enhances cell migration and epithelial-mesenchymal transition (EMT), offering therapeutic targets for lung diseases.
Area of Science:
- Immunology
- Cell Biology
- Respiratory Medicine
Background:
- Mycoplasma pneumoniae is a key respiratory pathogen causing pneumonia and asthma.
- Persistent infections can lead to lung fibrosis and airway abnormalities.
Purpose of the Study:
- Investigate signaling pathways regulating CCL20 expression after M. pneumoniae infection.
- Determine the impact of M. pneumoniae on cell migration and epithelial-mesenchymal transition (EMT).
Main Methods:
- THP-1 cells were infected with M. pneumoniae to measure CCL20 expression.
- Co-culture experiments with M. pneumoniae-infected THP-1 cells and bronchial epithelial cells assessed EMT and migration.
Main Results:
- M. pneumoniae infection upregulated CCL20 in THP-1 cells via the AKT-ERK1/2-AP1 pathway in a time- and dose-dependent manner.
- Co-culturing infected THP-1 cells with 16HBE cells promoted EMT and increased cell migration, linked to CCL20.
Conclusions:
- CCL20 plays a role in M. pneumoniae-induced cell migration and EMT.
- Understanding these mechanisms highlights potential therapeutic targets for M. pneumoniae-related lung diseases.
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