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DOI 10.1007/s00408-018-0166-y

Медицинская библиотека · Lung · 2018

Increased Sputum IL-17A Level in Non-asthmatic Eosinophilic Bronchitis.

Zhan Chen, Xu Rong, Liu Jiaxing, Zhang Shengfang, Luo Wei, Chen Ruchong, Lai Kefang

СтатьяПоддержка исследования: вне правительства СШАПеревод пока не подготовлен

Аннотация

BACKGROUND

Non-asthmatic eosinophilic bronchitis (NAEB) is one common cause of chronic cough which is characterized as airway eosinophilic inflammation like asthma but lack of airway hyper-responsiveness. Previous studies showed that Th2-pathway plays a role in NAEB, but the role of non-Th2 pathway in mechanism of NAEB remains unknown. Recently, IL-17A, a Th17-pathway cytokine, has been demonstrated to be involved in asthma development. However, the relationship between Th17-pathway and NAEB is unknown.

METHODS

We aim to assess the airway level of IL-17A in the subjects with NAEB. Relationships between the IL-17A level and airway function in NAEB or asthma are also observed. We measured IL-17A concentrations in the sputum supernatant from 12 subjects with EB, 16 subjects with asthma [9 eosinophilic asthmatic (EA) and 7 non-eosinophilic asthmatic (NEA) according to the sputum eosinophil ≥ 3%], and 9 healthy control subjects.

RESULTS

Increasing IL-17A level was found in NAEB group (29.65 ± 8.13 pg/ml), EA group (32.45 ± 3.22 pg/ml), and NEA group (29.62 ± 6.91 pg/ml) compared with the healthy control group (17.05 ± 10.30 pg/ml) (P < 0.05, P < 0.01, P < 0.05, respectively). The sputum IL-17A level was correlated with FENO (r = 0.44, P < 0.01), FEV1/FVC% (r = - 0.38, P < 0.05), MMEF%pred (r = - 0.34, P < 0.05), and sputum neutrophil% (r = 0.33, P < 0.05) in total.

CONCLUSION

Th17-pathway may play a role not only in asthmatics, but also in subjects with NAEB, as reflected by increasing IL-17A concentrations in sputum supernatant.

Для цитирования: Zhan Chen, Xu Rong, Liu Jiaxing, Zhang Shengfang, Luo Wei, Chen Ruchong, Lai Kefang. Increased Sputum IL-17A Level in Non-asthmatic Eosinophilic Bronchitis.. Lung. 2018. DOI: 10.1007/s00408-018-0166-y.

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