哮喘联盟

   摘要
   背景：气道嗜酸粒细胞性炎症是哮喘的主要特征，主要由2型反应驱动。Galectin-13在寄生虫感染模型中的表达上调，该模型的特征也是2型免疫反应。我们假设galectin-13可能与哮喘气道嗜酸粒细胞性炎症有关。
   目的：揭示Galectin-13在哮喘气道炎症中的作用。
   方法：我们检测了哮喘患者（n=54）和健康对照组（n=15）的支气管刷片、痰液和血浆中galectin-13的表达，并分析了galectin-13的表达与气道嗜酸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galectin-13参与嗜酸粒细胞性炎症的可能机制。
   结果：与对照组相比，哮喘患者的galectin-13表达显著增加。哮喘患者的上皮 galectin-13 mRNA水平与嗜酸粒细胞性气道炎症（痰嗜酸粒细胞百分比、支气管粘膜下层嗜酸粒细胞数量和FeNO）和 Th2型特征基因（CLCA1、POSTN和SERPINB2）的表达密切相关。吸入皮质类固醇（ICS）治疗降低了血浆galectin-13水平，基线血浆galectin-13水平反映了对ICS治疗的反应性。在培养的16HBE 细胞中，galectin-13的敲除通过抑制EGFR和ERK的激活来抑制IL-13诱导的MCP-1和eotaxin-1的表达。
   结论和临床相关性：Galectin-13是哮喘气道嗜酸粒细胞增多的新标志物，可能通过上调MCP-1和eotaxin-1的表达导致过敏性气道嗜酸粒细胞性炎症。血浆galectin-13水平可能有助于预测对ICS治疗的反应性。


 

(黄丹¹ 张红萍¹ 王刚² 四川大学华西医院中西医结合科呼吸病组 610041 摘译)
（Clin Exp Allergy. 2021 Dec;51(12):1566-1576.）

 
Increased epithelial galectin-13 expression associates with eosinophilic airway inflammation in asthma
 
Yi L, Zhang S, Feng Y, Wu W, Chang C, Chen D, Chen S, Zhao J, Zhen G.
Clin Exp Allergy. 2021 Dec;51(12):1566-1576. 
 
Abstract
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.
CONCLUSION & 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.