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首页> 外文期刊>Allergy >Chemerin suppresses murine allergic asthma by inhibiting CCL2 production and subsequent airway recruitment of inflammatory dendritic cells
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Chemerin suppresses murine allergic asthma by inhibiting CCL2 production and subsequent airway recruitment of inflammatory dendritic cells

机译：Chemerin通过抑制CCL2的产生并随后通过气道募集炎性树突细胞来抑制鼠类过敏性哮喘

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Background Chemerin has been implicated to play opposing roles, either pro-inflammatory or anti-inflammatory, in various tissue inflammation processes primarily through the regulation of tissue recruitment of immune cells. However, the effect of chemerin in allergic asthma has not yet been explored. We sought to investigate the role of chemerin in the murine model of allergic asthma and explore the underlying mechanism. Methods We examined the effect of intranasal (i.n.) administration of chemerin during antigen challenge in murine models of asthma. Moreover, we examined whether administration of CCL2 or bone marrow-derived dendritic cells (BMDCs) transfer reversed the effects of chemerin on ovalbumin-induced asthma. We finally examined the effect of chemerin on CCL2 expression in activated lung epithelial cells in vitro. Results The administration of chemerin attenuated allergic airway inflammation and airway hyperreactivity during antigen challenge. Chemerin treatment caused significant decreases in BALF CD4+ T-cell accumulation and mRNA expression of Th2-attracting chemokines, CCL17 and CCL22, which was accompanied by significantly decreased BALF CD11c+CD11b+ inflammatory DC accumulation and CCL2 production. Furthermore, airway administration of exogenous CCL2 or adoptive transfer of CD11c+CD11b+ BMDCs abrogated the suppressive effects of chemerin on allergic asthma. Finally, in vitro study showed that chemerin inhibited CCL2 secretion by low-dose LPS-stimulated lung epithelial cells, which led to decreased chemotaxis of BMDCs. Conclusions Our study demonstrates that chemerin plays a protective role in allergic asthma by suppressing airway recruitment of inflammatory CD11c +CD11b+ DCs through the inhibition of CCL2 secretion by active lung epithelial cells.
机译：背景技术凯莫瑞被暗示主要通过调节免疫细胞的组织募集而在各种组织炎症过程中发挥促炎或抗炎的相反作用。但是，尚未探讨凯莫瑞在过敏性哮喘中的作用。我们试图调查chemerin在小鼠过敏性哮喘模型中的作用，并探讨其潜在机制。方法我们检查了在哮喘小鼠模型中抗原激发期间鼻内（i.n.）施用凯莫瑞的效果。此外，我们检查了施用CCL2或骨髓源性树突状细胞（BMDC）是否能逆转凯莫瑞对卵清蛋白诱导的哮喘的作用。我们最终检查了凯莫瑞对体外活化的肺上皮细胞中CCL2表达的影响。结果凯莫瑞的使用减轻了抗原激发期间的过敏性气道炎症和气道高反应性。凯莫瑞处理导致BALF CD4 + T细胞积聚和吸引Th2的趋化因子CCL17和CCL22的mRNA表达显着降低，同时伴有BALF CD11c + CD11b +炎性DC积聚和CCL2产生显着降低。此外，气道给予外源性CCL2或CD11c + CD11b + BMDC的过继转移消除了凯莫瑞对过敏性哮喘的抑制作用。最后，体外研究表明，chemerin抑制了低剂量LPS​​刺激的肺上皮细胞的CCL2分泌，从而导致BMDC的趋化性降低。结论我们的研究表明chemerin通过抑制活性肺上皮细胞分泌CCL2来抑制炎症性CD11c + CD11b + DC的呼吸道募集，从而在过敏性哮喘中起保护作用。

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