Abstract
Background: Studies have shown that methyl-CpG binding domain protein 2 (MBD2) expression is significantly elevated in a neutrophil-dominant severe asthma mouse model. It also regulates Th17 cell differentiation. The objective of this study was to investigate the relationship between serum MBD2 levels in patients with severe asthma with different endotypes.Methods: Eligible adults with confirmed asthma (n = 63) underwent a clinical assessment, asthma control test and pulmonary function test and were classified as having mild, moderate or severe asthma. Severe asthma endotypes were defined according to the percentage of Th2 and Th17 cells in the peripheral blood and by the type of inflammation. The percentage of Th2 and Th17 cells in the peripheral blood was determined by flow cytometry. Serum MBD2, eosinophilic cationic protein and myeloperoxidase were measured by enzyme-linked immunosorbent assay. Correlations of MBD2 expression with clinical parameters were evaluated using Spearman's rank correlation analysis.Results: Serum MBD2 levels were upregulated in patients with severe asthma compared to healthy controls and patients with mild to moderate asthma. MBD2 was also significantly increased in patients with Th17 severe asthma compared to patients with type 2 severe asthma. Furthermore, MBD2 was positively correlated with MPO and Th17 cells but negatively correlated with ECP and Th2 cells in patients with severe asthma.Conclusions: These findings suggest that serum MBD2 may be a potential new biomarker for identifying severe asthma, Th17 severe asthma and the type of airway inflammation. However, these findings are still preliminary and need to be further investigated.
Highlights
Asthma is a highly heterogeneous and prevalent chronic respiratory disease that affects ∼300 million people worldwide [1]
In order to distinguish them from severe asthma, mild and moderate asthma was classified as “asthma.” Severe asthma endotypes were defined according to the percentage of T-helper cell type 2 (Th2) and T-helper cell type 17 (Th17) cells in the peripheral blood and by the type of inflammation, which were divided into type 2 (T2) severe asthma and Th17 severe asthma
The count of blood neutrophils was higher in Th17 severe asthma compared to T2 severe asthma, but the count of blood eosinophils was lower in Th17 severe asthma compared to T2 severe asthma. These findings suggest that the presence of T2 and non-T2 endotypes in asthma, with the latter being primarily mediated by Th17 cells and neutrophil infiltration, which is consistent with previous studies [8, 26, 27]
Summary
Asthma is a highly heterogeneous and prevalent chronic respiratory disease that affects ∼300 million people worldwide [1]. Studies have found that almost 50% of asthma cases show no infiltration of eosinophils (a non-T2 endotype) but are instead mainly infiltrated by neutrophils and insensitive to glucocorticoids. This pathway is mainly mediated by Th17 cells, known as Th17 asthma (or neutrophilic asthma) [7, 8]. Studies have shown that methyl-CpG binding domain protein 2 (MBD2) expression is significantly elevated in a neutrophil-dominant severe asthma mouse model. The objective of this study was to investigate the relationship between serum MBD2 levels in patients with severe asthma with different endotypes
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