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Variable p-CREB expression depicts different asthma phenotypes.

G Chiappara1, P Chanez, A Bruno

  • 1Istituto di Biomedicina e Immunologia Molecolare, Commessa di Immunopatologia e Farmacologia Sperimentale dell'Appartato Respiratorio, Consiglio Nazionale delle Ricerche, Palermo, Italy.

Allergy
|June 19, 2007
PubMed
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Asthma inflammation involves increased phospho-CREB (p-CREB) expression, particularly in severe, untreated cases. Glucocorticoids can reduce p-CREB levels in responsive asthma patients.

Area of Science:

  • Molecular Biology
  • Immunology
  • Respiratory Medicine

Background:

  • Chromatin modification influences inflammatory gene regulation in asthma.
  • Cyclic adenosine mono-phosphate response element-binding protein (CREB) and its co-activator CREB-binding protein (CBP) are implicated in pro-inflammatory gene transcription.

Purpose of the Study:

  • To assess the expression of CBP and phospho-CREB (p-CREB) in asthma patients.
  • To compare expression levels in bronchial biopsies and peripheral blood mononuclear cells (PBMC) across different asthma severity and treatment groups.

Main Methods:

  • Immunohistochemistry was used on bronchial biopsies.
  • Western blot and immunocytochemistry were performed on PBMC.
  • PBMC were also incubated in vitro with fluticasone propionate.

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Main Results:

  • p-CREB expression was significantly elevated in untreated and steroid-dependent asthmatic patients compared to controls and inhaled steroid-treated patients, in both bronchial epithelium and submucosa.
  • Increased p-CREB in the submucosa correlated positively with leukocyte infiltration (CD45RB+ cells).
  • In vitro, fluticasone propionate reduced cytokine-induced p-CREB expression in PBMC.

Conclusions:

  • p-CREB expression in asthma is linked to persistent inflammation and disease severity.
  • Glucocorticoids demonstrate a capacity to modulate p-CREB expression in responsive asthma patients.