Abstract：
OBJECTIVE: Since the leptin participates in the upregulation of type 2 innate lymphoid cells (ILC2s). We investigated the role of the leptin/ILC2 axis in AR pathogenesis in Chinese paediatric patients with obesity.
METHODS: Seventy AR paediatric patients with or without obesity and 30 healthy obese subjects were enrolled. The levels of leptin, its receptor and ILC2 milieu were measured, and correlations between them and clinical symptom severity and between ILC2 milieu and leptin levels were assessed. Changes of ILC2 milieu in AR patients after leptin stimulation were also detected.
RESULTS: Levels of leptin, its receptor and ILC2 milieu levels were significantly higher in the disease than in the controls, and highest in the obese-AR group. The leptin/ILC2 axis and severity of clinical symptoms in obese patients with AR were significantly correlated, similarly to what was observed between leptin/leptin receptors and ILC2 milieu. Recombinant leptin could significantly increased the levels of ILC2 milieu in the obese-AR group.
CONCLUSIONS: These findings suggest the unique function ofthe leptin/ILC2 axis in obese paediatric AR patients. The mechanism by which obesity promotes AR in paediatric patients may be related to the leptin/ILC2 axis.
METHODS: Seventy AR paediatric patients with or without obesity and 30 healthy obese subjects were enrolled. The levels of leptin, its receptor and ILC2 milieu were measured, and correlations between them and clinical symptom severity and between ILC2 milieu and leptin levels were assessed. Changes of ILC2 milieu in AR patients after leptin stimulation were also detected.
RESULTS: Levels of leptin, its receptor and ILC2 milieu levels were significantly higher in the disease than in the controls, and highest in the obese-AR group. The leptin/ILC2 axis and severity of clinical symptoms in obese patients with AR were significantly correlated, similarly to what was observed between leptin/leptin receptors and ILC2 milieu. Recombinant leptin could significantly increased the levels of ILC2 milieu in the obese-AR group.
CONCLUSIONS: These findings suggest the unique function ofthe leptin/ILC2 axis in obese paediatric AR patients. The mechanism by which obesity promotes AR in paediatric patients may be related to the leptin/ILC2 axis.
摘要：
目的：由于瘦素参与2型固有淋巴细胞（ILC2s）的上调。我们研究了瘦素/ILC2轴在中国肥胖儿童患者AR发病机制中的作用。
方法：纳入70例有或没有肥胖的AR儿科患者和30例健康肥胖受试者。瘦素水平,测量了它的受体和ILC2环境，并评估了它们与临床症状严重程度之间以及ILC2环境与瘦素水平之间的相关性。还检测了瘦素刺激后AR患者ILC2环境的变化。
结果：瘦素水平，该疾病的受体和ILC2环境水平明显高于对照组，肥胖AR组最高。瘦素/ILC2轴与肥胖AR患者临床症状严重程度显著相关,与在瘦素/瘦素受体和ILC2环境之间观察到的相似。重组瘦素可以显着增加肥胖-AR组的ILC2环境水平。
结论：这些发现提示瘦素/ILC2轴在肥胖儿童AR患者中的独特功能。肥胖促进儿科患者AR的机制可能与瘦素/ILC2轴有关。
方法：纳入70例有或没有肥胖的AR儿科患者和30例健康肥胖受试者。瘦素水平,测量了它的受体和ILC2环境，并评估了它们与临床症状严重程度之间以及ILC2环境与瘦素水平之间的相关性。还检测了瘦素刺激后AR患者ILC2环境的变化。
结果：瘦素水平，该疾病的受体和ILC2环境水平明显高于对照组，肥胖AR组最高。瘦素/ILC2轴与肥胖AR患者临床症状严重程度显著相关,与在瘦素/瘦素受体和ILC2环境之间观察到的相似。重组瘦素可以显着增加肥胖-AR组的ILC2环境水平。
结论：这些发现提示瘦素/ILC2轴在肥胖儿童AR患者中的独特功能。肥胖促进儿科患者AR的机制可能与瘦素/ILC2轴有关。
