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Corticosteroid modulation of immunoglobulin expression and B-cell function in COPD.

Jin Lee1, Matthew Machin1, Kirsty E Russell1

  • 1Airway Disease Section, National Heart and Lung Institute, Imperial College London, London, United Kingdom; and.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
|February 19, 2016
PubMed
Summary

Corticosteroid treatment in chronic obstructive pulmonary disease (COPD) altered gene expression, reducing immunoglobulin production and B-cell proliferation. Fluticasone propionate (FP) suppressed B-cell responses, suggesting efficacy in patients with high autoantibody titers.

Keywords:
DUSP1ERKLABAfluticasone propionate

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Area of Science:

  • Pulmonary Medicine
  • Immunology
  • Pharmacogenomics

Background:

  • Chronic obstructive pulmonary disease (COPD) involves complex immune dysregulation.
  • Corticosteroids are a cornerstone treatment for COPD, but their precise molecular effects on the immune system require further elucidation.

Purpose of the Study:

  • To investigate gene expression changes following corticosteroid treatment in COPD patients.
  • To identify the regulatory mechanisms behind these gene expression alterations.
  • To assess the impact of fluticasone propionate (FP) on immunoglobulin G (IgG) expression and B-cell function.

Main Methods:

  • Gene expression profiling using microarrays and validation via real-time reverse transcription-quantitative PCR (RT-qPCR).
  • Analysis of biopsy samples from Global Initiative for Chronic Obstructive Lung Disease (GOLD) stage I-II COPD patients before and after fluticasone propionate/salmeterol (FP/SM) treatment.
  • In vitro studies examining FP's effect on B-cell proliferation and IgG expression under oxidative stress.

Main Results:

  • FP/SM treatment significantly altered gene expression, up-regulating 180 genes and down-regulating 343 genes.
  • Down-regulated genes were primarily associated with immunoglobulin production; FK506 binding protein (FK506BP) was up-regulated.
  • FP reduced IgG expression and B-cell proliferation by increasing dual-specificity protein phosphatase 1 (DUSP1) expression, leading to ERK-1/2 dephosphorylation, an effect not prevented by oxidative stress.

Conclusions:

  • Corticosteroid therapy, specifically FP, may modulate the adaptive immune response in COPD by suppressing immunoglobulin production and B-cell function.
  • FP's effectiveness might be greater in COPD patients exhibiting a heightened B-cell/antibody response, as indicated by elevated autoantibody titers.