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Looking for Airways Periostin in Severe Asthma: Could It Be Useful for Clustering Type 2 Endotype?
Chest 2018 November
BACKGROUND: Severe asthma is heterogeneous clinically and biologically and is often difficult to control. In particular, the type 2 (T2) immunity endotype of severe asthma is gaining increasing interest because it is susceptible to newly developed biologic treatments that can transform the quality of life of these patients. The aim of this study was to analyze periostin concentrations in the airways of patients with severe asthma, evaluating its role in clustering the T2 endotype.
METHODS: We enrolled 40 consecutive patients with severe asthma (T2 endotype: n = 25; non-T2 endotype: n = 15), 21 patients with mild to moderate asthma, and 15 healthy control subjects. All subjects enrolled underwent exhaled breath condensate (EBC) and sputum collection, eosinophil count in blood, fractional exhaled nitric oxide, and IgE measurement. Periostin was assessed by an enzyme-linked immunosorbent assay kit on EBC and induced sputum (IS) supernatant.
RESULTS: We were able to detect higher periostin levels in the EBC (0.75 ± 0.46 vs 0.70 ± 0.19 vs 0.11 ± 0.05 ng/mL, P < .05 and P < .01) and in IS (0.55 ± 0.23 vs 0.31 ± 0.13 vs 0.16 ± 0.120 ng/mL, P < .05 and P < .01) of patients with severe asthma compared with patients with mild to moderate asthma and healthy control subjects, respectively. We further found an increase of periostin levels in both samples in T2 endotype compared with non-T2 endotype (EBC: 0.88 ± 0.46 vs 0.52 ± 0.46 ng/mL; IS: 0.69 ± 0.19 vs 0.39 ± 0.16 ng/mL; P < .05) and a correlation between periostin levels in EBC and sputum.
CONCLUSIONS: We found that periostin is measurable in the airways and increased in patients with severe asthma, especially in those from the T2 endotype. Unlike serum periostin, which may be derived from several sources outside the lung, airways periostin is a useful marker of severe eosinophilic asthma and may help to phenotype patients that will respond to the biologic agents.
METHODS: We enrolled 40 consecutive patients with severe asthma (T2 endotype: n = 25; non-T2 endotype: n = 15), 21 patients with mild to moderate asthma, and 15 healthy control subjects. All subjects enrolled underwent exhaled breath condensate (EBC) and sputum collection, eosinophil count in blood, fractional exhaled nitric oxide, and IgE measurement. Periostin was assessed by an enzyme-linked immunosorbent assay kit on EBC and induced sputum (IS) supernatant.
RESULTS: We were able to detect higher periostin levels in the EBC (0.75 ± 0.46 vs 0.70 ± 0.19 vs 0.11 ± 0.05 ng/mL, P < .05 and P < .01) and in IS (0.55 ± 0.23 vs 0.31 ± 0.13 vs 0.16 ± 0.120 ng/mL, P < .05 and P < .01) of patients with severe asthma compared with patients with mild to moderate asthma and healthy control subjects, respectively. We further found an increase of periostin levels in both samples in T2 endotype compared with non-T2 endotype (EBC: 0.88 ± 0.46 vs 0.52 ± 0.46 ng/mL; IS: 0.69 ± 0.19 vs 0.39 ± 0.16 ng/mL; P < .05) and a correlation between periostin levels in EBC and sputum.
CONCLUSIONS: We found that periostin is measurable in the airways and increased in patients with severe asthma, especially in those from the T2 endotype. Unlike serum periostin, which may be derived from several sources outside the lung, airways periostin is a useful marker of severe eosinophilic asthma and may help to phenotype patients that will respond to the biologic agents.
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