Yi Lingling, Zhang Shuchen, Feng Yuchen, Wu Wenliang, Chang Chenli, Chen Dian, Chen Shengchong, Zhao Jianping, Zhen Guohua
Division of Respiratory and Critical Care Medicine, Department of Internal Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Key Laboratory of Respiratory Diseases, National Health Commission of People's Republic of China, Wuhan, China.
Clin Exp Allergy. 2021 Dec;51(12):1566-1576. doi: 10.1111/cea.13961. Epub 2021 Jun 19.
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.
To unveil the role of galectin-13 in asthma airway inflammation.
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.
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.
气道嗜酸性粒细胞炎症是哮喘的核心特征，主要由2型反应驱动。半乳糖凝集素-13在寄生虫感染模型中的表达上调，该模型也以2型免疫反应为特征。我们推测半乳糖凝集素-13可能参与哮喘气道嗜酸性粒细胞炎症。
揭示半乳糖凝集素-13在哮喘气道炎症中的作用。
我们检测了哮喘患者（n = 54）和健康对照者（n = 15）支气管刷检物、痰液和血浆中的半乳糖凝集素-13表达，并分析了半乳糖凝集素-13表达与气道嗜酸性粒细胞增多之间的相关性。我们使用人支气管上皮细胞系16HBE来研究半乳糖凝集素-13参与嗜酸性粒细胞炎症的可能机制。
与对照组相比，哮喘患者中半乳糖凝集素-13的表达明显增加。哮喘患者上皮半乳糖凝集素-13 mRNA水平与嗜酸性气道炎症（痰液嗜酸性粒细胞百分比、支气管黏膜下层嗜酸性粒细胞数量和呼出一氧化氮）以及Th2特征基因（CLCA1、POSTN和SERPINB2）的表达密切相关。吸入糖皮质激素（ICS）治疗可降低血浆半乳糖凝集素-13水平，基线血浆半乳糖凝集素-13水平反映对ICS治疗的反应。在培养的16HBE细胞中，敲低半乳糖凝集素-13可通过抑制EGFR和ERK的激活来抑制IL-13刺激的MCP-1和嗜酸性粒细胞趋化因子-1表达。
半乳糖凝集素-13是哮喘气道嗜酸性粒细胞增多的新型标志物，可能通过上调MCP-1和嗜酸性粒细胞趋化因子-1的表达促进过敏性气道嗜酸性粒细胞炎症。血浆半乳糖凝集素-13水平可能有助于预测对ICS治疗的反应。
