Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2021
Increased epithelial galectin-13 expression associates with eosinophilic airway inflammation in asthma.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Yi Lingling, Zhang Shuchen, Feng Yuchen, Wu Wenliang, Chang Chenli, Chen Dian, Chen Shengchong, Zhao Jianping, Zhen Guohua
Аннотация
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.
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.