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.

Abstract

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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