Background
Airway eosinophilic inflammation is a central feature in asthma which is mainly driven by type 2 response. The expression of galectin‐13 was up‐regulated in a parasitic infection model which is also characterized by type 2 immune response. We hypothesized that galectin‐13 may be involved in airway eosinophilic inflammation in asthma.
Objective
To unveil the role of galectin‐13 in asthma airway inflammation.
Methods
We measured galectin‐13 expressions in bronchial brushings, sputum, and plasma of asthma patients (n = 54) and healthy controls (n = 15), and analysed the correlations between galectin‐13 expression and airway eosinophilia. We used human bronchial epithelial cell line 16HBE to investigate the possible mechanism by which galectin‐13 participates in eosinophilic inflammation.
Results
The expression of galectin‐13 was markedly increased in subjects with asthma compared to controls. Epithelial galectin‐13 mRNA levels in asthmatic subjects were strongly correlated with eosinophilic airway inflammation (the percentage of sputum eosinophils, the number of eosinophils in bronchial submucosa and FeNO) and the expression of Th2 signature genes (CLCA1, POSTN and SERPINB2). Inhaled corticosteroid (ICS) treatment reduced plasma galectin‐13 levels, and baseline plasma galectin‐13 levels reflect the response to ICS treatment. In cultured 16HBE cells, knockdown of galectin‐13 suppressed IL‐13‐stimulated MCP‐1 and eotaxin‐1 expression by inhibiting the activation of EGFR and ERK.
Conclusions & Clinical Relevance
Galectin‐13 is a novel marker for airway eosinophilia in asthma, and may contribute to allergic airway eosinophilic inflammation by up‐regulating the expression of MCP‐1 and eotaxin‐1. Plasma galectin‐13 levels may be useful for predicting responses to ICS treatment.
<b><i>Introduction:</i></b> Asymptomatic sensitization is defined as the presence of positive skin prick test (SPT) and/or positive serum allergen-specific IgE in the absence of clinical allergic symptoms. Currently, there is no convincing explanation why some people with positive allergen tests do not show symptoms. We aimed to investigate the house dust mite (HDM)-specific IgE and IgG4 repertoire in asymptomatic HDM-sensitized subjects and HDM-induced allergic rhinitis (AR) patients. <b><i>Methods:</i></b> A total of 48 subjects sensitized to HDM were included in this study: 27 had AR with/without asthma (symptomatic group), and 21 had no allergic symptoms (asymptomatic group). Six healthy individuals served as control group. Peripheral blood samples were collected for serum IgE and IgG4 assay and basophil activation tests (BATs). IgE and IgG4 assay included antibodies to <i>Dermatophagoides</i> (<i>Der</i>) <i>p1</i>, <i>2</i>, <i>7</i>, <i>10</i>, <i>21</i>, <i>23</i>, and <i>Der f1</i>, <i>2</i>. <b><i>Results:</i></b> AR patients had a larger wheal diameter of SPT (7.0 vs. 3.0 mm, <i>p</i> < 0.0001) and a higher specific IgE to <i>Der p</i> (15.50 vs. 0.70 KU/L, <i>p</i> < 0.0001) than asymptomatic subjects. They also showed more frequent sensitization to <i>Der p1</i> and <i>Der p2</i> (both <i>p</i> < 0.05). However, the total IgE and specific IgG4 did not differ significantly between the 2 groups. The basophil activation response after being stimulated with HDM was observed to be higher in AR patients (all <i>p</i> < 0.05). <b><i>Conclusions:</i></b> There are differences in SPT, serum-specific IgE to <i>Der p</i>, component allergen <i>Der p1</i> and <i>Der p2</i> level and BAT between AR patients and asymptomatic subjects sensitized to HDM. IgG4 alone cannot differentiate asymptomatic individuals from AR patients.
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