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Serum periostin does not reflect type 2-driven inflammation in COPD
O A Carpaij1,2, F O W Muntinghe3, M B Wagenaar3
1University of Groningen, University Medical Center Groningen, Groningen Research Institute for Asthma and COPD (GRIAC), Groningen, The Netherlands. o.a.carpaij@umcg.nl.
Respiratory Research
|June 9, 2018
Summary
Serum periostin is elevated in chronic obstructive pulmonary disease (COPD) patients compared to healthy individuals. However, periostin does not effectively predict Th2-driven inflammation or inhaled corticosteroid (ICS) response in COPD.
Area of Science:
- Pulmonary Medicine
- Immunology
- Biomarker Discovery
Background:
- Chronic obstructive pulmonary disease (COPD) involves Th2-driven inflammation, but affected patient subgroups remain unclear.
- Periostin, linked to Th2 inflammation and inhaled corticosteroid (ICS) response in asthma, was investigated as a potential COPD biomarker.
- The study aimed to assess serum periostin levels in COPD patients versus controls, its relation to smoking status, inflammatory markers, and ICS responsiveness.
Discussion:
- COPD smokers and past-smokers exhibited significantly higher serum periostin levels than healthy smokers.
- No significant correlation was found between serum periostin and inflammatory cell counts in blood, sputum, or endobronchial biopsies in COPD patients.
- Serum periostin levels did not correlate with age or FEV1% predicted in COPD patients, unlike in healthy smokers.
Key Insights:
- Serum periostin is elevated in COPD patients, irrespective of smoking status, compared to healthy controls.
- Periostin levels in COPD do not correlate with key inflammatory markers or predict ICS treatment response.
- The findings suggest periostin is not a suitable biomarker for Th2-driven inflammation or ICS responsiveness in COPD.
Outlook:
- Further research is needed to identify reliable biomarkers for Th2-driven inflammation in COPD.
- Exploring other potential biomarkers could aid in stratifying COPD patients for targeted therapies.
- Understanding the role of periostin in COPD pathogenesis warrants further investigation beyond its potential as a predictive biomarker.
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