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Peptidoglycan from Staphylococcus aureus increases MUC5AC gene expression via RSK1-CREB pathway in human airway

Young Ok Kim1, Min Jung Jung, Jang Kyu Choi

  • 1Department of Physiology, Kosin University College of Medicine, Busan 602-703, Korea.

Molecules and Cells
|September 10, 2011
PubMed

Insights

Staphylococcus aureus peptidoglycan (PGN) triggers MUC5AC gene expression in airways. This process involves ERK1/2 and RSK1 signaling pathways, ultimately activating CREB and leading to increased MUC5AC transcription.

Area of Science:

  • Pulmonary medicine
  • Molecular biology
  • Immunology

Background:

  • Respiratory infections and pollutants can cause pulmonary diseases.
  • Mucous overproduction is a key feature of these diseases.
  • Staphylococcus aureus peptidoglycan (PGN) is known to induce MUC5AC overexpression.

Purpose of the Study:

  • To elucidate the molecular mechanisms underlying PGN-induced MUC5AC gene expression in the airway.
  • To identify the specific signaling pathways involved in this process.

Main Methods:

  • NCI-H292 cells were treated with PGN.
  • Time- and dose-dependent effects of PGN on MUC5AC expression were assessed.
  • Activation of MAP kinases (ERK1/2, JNK, p38) and RSK1 was evaluated.
  • Pharmacological inhibitors (PD98059) were used to block specific pathways.
  • CREB phosphorylation and MUC5AC promoter activity were analyzed.

Main Results:

  • PGN induced MUC5AC gene expression in a time- and dose-dependent manner.
  • ERK1/2 and JNK pathways were activated by PGN, while p38 was not.
  • Inhibition of ERK1/2 reduced PGN-induced MUC5AC expression.
  • RSK1 activation was downstream of ERK1/2 and mediated PGN effects.
  • RSK1 activation led to CREB phosphorylation and MUC5AC transcription.
  • The cAMP-response element (CRE) in the MUC5AC promoter was crucial.

Conclusions:

  • PGN induces MUC5AC gene expression via the ERK1/2-RSK1-CREB signaling pathway.
  • This pathway is critical for PGN-mediated mucous overproduction in airway cells.
  • Understanding this mechanism offers potential therapeutic targets for related pulmonary diseases.

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