TY - JOUR A2 - Fröde, Tânia Silvia AU - Zhang, Yingli AU - Liang, Rongrong AU - Xie, Aicen AU - Shi, Wenqian AU - Huang, Huarong AU - ZhongYingqiang PY - 2020 DA - 2020/04/28 TI -拮抗肽专门绑定到第一和第二CCR5和Anti-IL-23p19抗体减少气道炎症的细胞外循环通过抑制IL-23 / Th17信号通路SP - 1719467六世- 2020 AB -哮喘是一种异构的气道慢性炎症性疾病病因复杂，涉及多种细胞和细胞成分。因此，本研究的目的是研究特异性结合CCR5的第一和第二胞外环(GH和HY多肽，从而介导哮喘小鼠的炎症反应和IL-23/T辅助17 (Th17)细胞通路。用卵白蛋白(OVA)诱导BALB/c小鼠模型，用抗CCR5或抗il -23p19的多肽治疗。评估哮喘炎症和粘液产生的程度。收集支气管肺泡灌洗液(BALF)，计数细胞，ELISA检测IL-4水平。检测肺组织中IL-23/Th17通路相关蛋白和mRNA水平，检测胸腺、脾脏和外周血中Th17细胞的阳性生成率。两种多肽和/或抗il -23p19治疗组的过敏性炎症和粘液分泌明显减少; decreased expression levels of IL-23p19, IL-23R, IL-17A and lactoferrin (LTF); and reduced proportions of Th17 cells in the thymus, spleen, and peripheral blood. Specifically, among the four treatment groups, the anti-IL-23p19 with HY peptide group exhibited the lowest positive production rate of Th17 cells. Our data also showed a significant and positive correlation between CCR5 and IL-23p19 protein expression. These findings suggest that the administration of peptides antagonistic to CCR5 and/or anti-IL-23p19 can reduce airway inflammation in asthmatic mice, most likely through inhibition of the IL-23/Th17 signaling pathway, and the HY peptide can alleviate inflammation not only through the IL-23/Th17 pathway but also through other mechanisms that result in the regulation of inflammation. SN - 0962-9351 UR - https://doi.org/10.1155/2020/1719467 DO - 10.1155/2020/1719467 JF - Mediators of Inflammation PB - Hindawi KW - ER -