Elevation of anti-elastin antibody in patients with asthma

哮喘患者抗弹性蛋白抗体升高

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作者:Shingo Tokita, Kumiya Sugiyama, Tomoshige Wakayama, Hajime Arifuku, Naotatsu Otsuji, Kei Sugitate, Takayoshi Owada, Kenya Koyama, Hirokuni Hirata, Masafumi Arima, Yoshihiko Ueda, Yasutsugu Fukushima

Background

It is often difficult to differentiate between asthma and chronic obstructive pulmonary disease (COPD), and useful biomarkers are needed for accurate diagnosis.

Conclusions

Anti-elastin Ab in sputum could be a useful biomarker for COPD and asthma in ever-smokers. In asthma, anti-elastin Ab was recruited to the airways by both airway allergic inflammation and smoking, and it may contribute to the progression of airway remodeling via autoimmune inflammation, but not emphysema, in COPD.

Methods

Patients with asthma (male to female ratio = 10/13; mean age, 67.3 years), COPD (16/0; 74.8 years) and controls (8/4; 72.3 years) were enrolled. Samples from sputum and serum were collected and levels of anti-elastin Ab were measured.

Objective

We evaluated anti-elastin antibody to identify useful biomarkers for differentiating between a diagnosis of asthma and COPD.

Results

The levels of anti-elastin Ab in sputum were significantly higher in asthma (11.4 ± 7.16 μg/mL) than in COPD (5.82 ± 5.16 μg/mL; P < 0.01), and serum levels in asthma (67.4 ± 29.7 μg/mL) were also significantly higher than in COPD or controls (45.0 ± 12.8 μg/mL; P < 0.05, 38.6 ± 10.4 μg/mL; P < 0.01, respectively). Anti-elastin Ab in sputum showed a positive correlation with smoking in asthma (r2 = 0.218, P < 0.05). However, no significant differences were observed in the levels of anti-elastin Ab and eosinophils, asthma phenotypes, inhaled corticosteroids, or severity in patients with asthma. Elastin was strongly expressed under the airway basement membrane in asthma compared with COPD or the healthy control. Conclusions: Anti-elastin Ab in sputum could be a useful biomarker for COPD and asthma in ever-smokers. In asthma, anti-elastin Ab was recruited to the airways by both airway allergic inflammation and smoking, and it may contribute to the progression of airway remodeling via autoimmune inflammation, but not emphysema, in COPD.

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