Sudharson Srinidhi, Eckl-Dorna Julia, Meshcheryakova Anastasia, Basílio José, Derdak Sophia, Kalic Tanja, Lengger Nina, Schweitzer Nina, Mechtcheriakova Diana, Breiteneder Heimo, Hafner Christine
Department of Dermatology, University Hospital St. Poelten, Karl Landsteiner University of Health Sciences, St. Poelten, Austria.
Department of Pathophysiology and Allergy Research, Center of Pathophysiology, Infectiology and Immunology, Medical University of Vienna, Vienna, Austria.
Allergy. 2025 Jun;80(6):1757-1769. doi: 10.1111/all.16448. Epub 2024 Dec 24.
Birch pollen (BP) interacts with airway epithelial cells to cause allergic sensitization and allergy in predisposed individuals. However, the basic mechanisms underlying the clinical effects are poorly understood. Changes in gene expression and cytokine secretion in nasal mucosal cells upon BP exposure were determined in BP-allergic and non-allergic individuals.
BP-allergic (n = 11) and non-allergic individuals (n = 12) participated in nasal provocations with saline and aqueous BP solution. Nasal scrapings and secretions were obtained at baseline and after BP provocation. Bulk RNA sequencing of the nasal scrapings was performed, and cytokines in nasal secretions were quantified.
After BP challenge, we identified 160 differentially expressed genes (DEGs) in the nasal scrapings of allergic individuals and 44 in non-allergic individuals. DEGs encoding S100 proteins, keratins, small proline-rich repeat proteins, and cytokines were predominantly identified, with proinflammatory cytokine transcripts being upregulated only in the allergic cohort. The top canonical pathways in allergic individuals included granulocyte and agranulocyte adhesion and diapedesis, wound healing, IL-8 signaling, and IL-17-related pathways. Enriched pathways in allergic participants were associated with granulocyte chemotaxis, humoral cell responses, and IL-10, IL-4, and IL-13 signaling and were absent in non-allergic individuals. At baseline and after BP challenge, higher amounts of CCL17, CCL20, CCL26, IL-7, IL-16, and IL-33 were detected in nasal secretions of allergic compared to non-allergic individuals.
Our results highlight the activation of important cellular signaling pathways specific to BP-allergic individuals after BP exposure offering new perspectives for studying key players in BP allergy.
桦树花粉（BP）与气道上皮细胞相互作用，在易感个体中引发过敏致敏和过敏反应。然而，其临床效应的基本机制尚不清楚。本研究确定了BP过敏和非过敏个体在接触BP后鼻黏膜细胞中基因表达和细胞因子分泌的变化。
BP过敏个体（n = 11）和非过敏个体（n = 12）参与了用生理盐水和BP水溶液进行的鼻激发试验。在基线和BP激发后获取鼻刮片和分泌物。对鼻刮片进行大量RNA测序，并对鼻分泌物中的细胞因子进行定量分析。
BP激发后，我们在过敏个体的鼻刮片中鉴定出160个差异表达基因（DEG），在非过敏个体中鉴定出44个。主要鉴定出编码S100蛋白、角蛋白、富含脯氨酸的小重复蛋白和细胞因子的DEG，促炎细胞因子转录本仅在过敏组中上调。过敏个体中排名靠前的典型通路包括粒细胞和无粒细胞黏附与渗出、伤口愈合、IL-8信号通路和IL-17相关通路。过敏参与者中富集的通路与粒细胞趋化性、体液细胞反应以及IL-10、IL-4和IL-13信号通路相关，在非过敏个体中不存在。与非过敏个体相比，在基线和BP激发后，过敏个体的鼻分泌物中检测到更高水平的CCL17、CCL20、CCL26、IL-7、IL-16和IL-33。
我们的结果突出了BP暴露后BP过敏个体特有的重要细胞信号通路的激活，为研究BP过敏的关键因素提供了新的视角。
