IL-25 likely has vital roles in initiating and activating type-2 immune responses in AR. We hypothesized that the molecules produced IL-25 by allergen-producing organisms such as JC is involved in the pathogenesis of AR. Participants included 13 patients with Japanese cedar pollinosis and 10 HCs. We measured the IL-25 protein concentration in nasal secretions and in culture supernatants of PNECs. NHBE cells were stimulated with pharmacological and immunological agents and JC. The IL-25 concentration in nasal secretions was significantly higher in patients with Japanese cedar pollinosis than in HCs. JC stimulated IL-25 production from PNECs. TNF-α, IL-4, and IL-13 significantly enhanced JC-induced IL-25 production; their activation by serine proteases was sufficient to enhance IL-25 production. Furthermore, the NADPH oxidase activity, including JC enhanced IL-25 production. A better understanding of JC-induced IL-25 production by epithelial cells may allow the development of novel therapeutic and preventive strategies for Japanese cedar pollinosis.

IL-25可能在AR中引发和激活2型免疫应答中起着至关重要的作用。我们假设由过敏原产生生物（如JC）产生IL-25的分子参与了AR的发病机理。参加者包括13例日本雪松花粉病和10例HCs。我们测量了鼻分泌物和PNECs培养上清液中的IL-25蛋白浓度。NHBE细胞用药理和免疫试剂以及JC刺激。日本柳杉花粉病患者鼻分泌物中的IL-25浓度显着高于HCs。JC刺激了PNEC产生IL-25。TNF-α，IL-4和IL-13显着增强JC诱导的IL-25产生; 它们被丝氨酸蛋白酶激活足以增强IL-25的产生。此外，包括JC在内的NADPH氧化酶活性增强了IL-25的产生。上皮细胞对JC诱导的IL-25产生的更好理解可能会为日本雪松花粉病提供新的治疗和预防策略。