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Antagonism of the prostaglandin D2 receptor CRTH2 attenuates asthma pathology in mouse eosinophilic airway inflammation

机译:前列腺素D2受体CRTH2的拮抗作用减弱了小鼠嗜酸性气道炎症中的哮喘病理

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摘要

BackgroundMast cell-derived prostaglandin D2 (PGD2), may contribute to eosinophilic inflammation and mucus production in allergic asthma. Chemoattractant receptor homologous molecule expressed on TH2 cells (CRTH2), a high affinity receptor for prostaglandin D2, mediates trafficking of TH2-cells, mast cells, and eosinophils to inflammatory sites, and has recently attracted interest as target for treatment of allergic airway diseases. The present study involving mice explores the specificity of CRTH2 antagonism of TM30089, which is structurally closely related to the dual TP/CRTH2 antagonist ramatroban, and compares the ability of ramatroban and TM30089 to inhibit asthma-like pathology.
机译:背景肥大细胞源性前列腺素D2(PGD2)可能导致变应性哮喘中嗜酸性粒细胞炎症和粘液产生。在TH2细胞(CRTH2)上表达的趋化性受体同源分子(CRTH2)是前列腺素D2的高亲和力受体,介导TH2细胞,肥大细胞和嗜酸性粒细胞向炎症部位的转运,最近引起了人们的兴趣,作为治疗过敏性气道疾病的靶标。本项涉及小鼠的研究探讨了TM30089的CRTH2拮抗作用的特异性,它在结构上与TP / CRTH2双重拮抗剂ramatroban密切相关,并比较了ramatroban和TM30089抑制哮喘样病理的能力。

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