Serum periostin does not reflect type 2-driven inflammation in COPD.

Although Th2 driven inflammation is present in COPD, it is not clearly elucidated which COPD patients are affected. Since periostin is associated with Th2 driven inflammation and inhaled corticosteroid (ICS)-response in asthma, it could function as a biomarker in COPD. The aim of this study was to analyze if serum periostin is elevated in COPD compared to healthy controls, if it is affected by smoking status, if it is linked to inflammatory cell counts in blood, sputum and endobronchial biopsies, and if periostin can predict ICS-response in COPD patients.Serum periostin levels were measured using Elecsys Periostin immunoassay. Correlations between periostin and inflammatory cell count in blood, sputum and endobronchial biopsies were analyzed. Additionally, the correlation between serum periostin levels and treatment responsiveness after 6 and 30 months was assessed using i.e. ΔFEV1% predicted, ΔCCQ score and ΔRV/TLC ratio. Forty-five COPD smokers, 25 COPD past-smokers, 22 healthy smokers and 23 healthy never-smokers were included. Linear regression analysis of serum periostin showed positive correlations age (B = 0.02, 95%CI 0.01-0.03) and FEV1% predicted (B = 0.01, 95%CI 0.01-0.02) in healthy smokers, but not in COPD patients In conclusion, COPD -smokers and -past-smokers have significantly higher periostin levels compared to healthy smokers, yet periostin is not suitable as a biomarker for Th2-driven inflammation or ICS-responsiveness in COPD.

Recipient gene polymorphisms in the Th-1 cytokines IL-2 and IFN-gamma in relation to acute rejection and graft vascular disease after clinical heart transplantation.

IL-2 and IFN-gamma are associated with acute rejection (AR) and graft vascular disease (GVD) after clinical heart transplantation. Polymorphisms in the genes of IL-2 (T-330G in the promoter) and IFN-gamma (CA repeat in the first intron) influence the production levels of these cytokines. Therefore, these polymorphisms might have an effect on the outcome after transplantation. To investigate possible effects of genetic variations in IL-2 and IFN-gamma genes on AR and GVD, we analyzed the IL-2 T-330G and the IFN-gamma CA repeat polymorphism in DNA of 301 heart transplant recipients. No associations were found for allele or genotype distributions between patients with or without AR (IL-2 allele frequency: P=0.44, genotype distribution: P=0.46; IFN-gamma allele frequency P=0.10, genotype distribution 12 repeats allele: P=0.21). Also, no associations were found analyzing the number (0 vs. 1 vs. >or=1) of AR (IL-2 allele frequency: P=0.59; genotype distribution: P=0.37; IFN-gamma allele frequency: P=0.27, genotype distribution 12 repeats allele: P=0.41) or analyzing the polymorphisms in patients with AR within the first month or thereafter (IL-2 allele frequency: P=0.45, genotype distribution: P=0.38; IFN-gamma allele frequency: P=0.21, genotype distribution 12 repeats allele: P=0.41). Analyzing both polymorphisms in relation to GVD, resulted in comparable allele and genotype distributions (IL-2 allele frequency: P=0.75; genotype distribution: P=0.77; IFN-gamma allele frequency: P=0.70, genotype distribution 12 repeats allele: P=0.63). In conclusion, we did not detect an association between the IL-2 T-330G promoter polymorphism and CA repeat polymorphism in the first intron of the IFN-gamma gene and AR or GVD after heart transplantation.