Abstract：
BACKGROUND: Prostaglandin D2 (PGD2), which is produced mainly by Th2 cells and mast cells, promotes a type-2 immune response by activating Th2 cells, mast cells, eosinophils, and group 2 innate lymphoid cells (ILC2s) via its receptor, chemoattractant receptor-homologous molecules on Th2 cells (CRTH2). However, the role of CRTH2 in models of airway inflammation induced by sensitization without adjuvants, in which both IgE and mast cells may play major roles, remain unclear.
METHODS: Wild-type (WT) and CRTH2-knockout (KO) mice were sensitized with ovalbumin (OVA) without an adjuvant and then challenged intranasally with OVA. Airway inflammation was assessed based on airway hyperresponsiveness (AHR), lung histology, number of leukocytes, and levels of type-2 cytokines in the bronchoalveolar lavage fluid (BALF).
RESULTS: AHR was significantly reduced after OVA challenge in CRTH2 KO mice compared to WT mice. The number of eosinophils, levels of type-2 cytokines (IL-4, IL-5, and IL-13) in BALF, and IgE concentration in serum were decreased in CRTH2 KO mice compared to WT mice. However, lung histological changes were comparable between WT and CRTH2 KO mice.
CONCLUSIONS: CRTH2 is responsible for the development of asthma responses in a mouse model of airway inflammation that features prominent involvement of both IgE and mast cells.
METHODS: Wild-type (WT) and CRTH2-knockout (KO) mice were sensitized with ovalbumin (OVA) without an adjuvant and then challenged intranasally with OVA. Airway inflammation was assessed based on airway hyperresponsiveness (AHR), lung histology, number of leukocytes, and levels of type-2 cytokines in the bronchoalveolar lavage fluid (BALF).
RESULTS: AHR was significantly reduced after OVA challenge in CRTH2 KO mice compared to WT mice. The number of eosinophils, levels of type-2 cytokines (IL-4, IL-5, and IL-13) in BALF, and IgE concentration in serum were decreased in CRTH2 KO mice compared to WT mice. However, lung histological changes were comparable between WT and CRTH2 KO mice.
CONCLUSIONS: CRTH2 is responsible for the development of asthma responses in a mouse model of airway inflammation that features prominent involvement of both IgE and mast cells.
摘要：
背景：前列腺素D2（PGD2），主要由Th2细胞和肥大细胞产生，通过激活Th2细胞促进2型免疫反应，肥大细胞,嗜酸性粒细胞,和第2组先天淋巴细胞（ILC2s）通过其受体，Th2细胞（CRTH2）上的化学引诱物受体同源分子。然而,CRTH2在无佐剂致敏诱导的气道炎症模型中的作用，其中IgE和肥大细胞可能起主要作用，仍然不清楚。
方法:野生型(WT)和CRTH2敲除(KO)小鼠用无佐剂的卵清蛋白(OVA)致敏,然后用OVA鼻内攻击。根据气道高反应性（AHR）评估气道炎症，肺组织学,白细胞的数量，以及支气管肺泡灌洗液（BALF）中2型细胞因子的水平。
结果：与WT小鼠相比，CRTH2KO小鼠的OVA攻击后AHR显着降低。嗜酸性粒细胞的数量，BALF中2型细胞因子（IL-4，IL-5和IL-13）的水平，与WT小鼠相比，CRTH2KO小鼠的血清中IgE浓度降低。然而,WT和CRTH2KO小鼠的肺组织学变化相当。
结论：在气道炎症小鼠模型中，CRTH2与哮喘反应的发展有关，该模型的特征是IgE和肥大细胞的明显受累。
方法:野生型(WT)和CRTH2敲除(KO)小鼠用无佐剂的卵清蛋白(OVA)致敏,然后用OVA鼻内攻击。根据气道高反应性（AHR）评估气道炎症，肺组织学,白细胞的数量，以及支气管肺泡灌洗液（BALF）中2型细胞因子的水平。
结果：与WT小鼠相比，CRTH2KO小鼠的OVA攻击后AHR显着降低。嗜酸性粒细胞的数量，BALF中2型细胞因子（IL-4，IL-5和IL-13）的水平，与WT小鼠相比，CRTH2KO小鼠的血清中IgE浓度降低。然而,WT和CRTH2KO小鼠的肺组织学变化相当。
结论：在气道炎症小鼠模型中，CRTH2与哮喘反应的发展有关，该模型的特征是IgE和肥大细胞的明显受累。
