在喘小鼠中,抗S100A4抗体的使用缓解了支气管上皮质-介质细胞过渡
Shuang Liu1, Min Liu1, Jinnan Zhong1
1Department of Respiratory and Critical Care Medicine, Affiliated Hospital of Jianghan University, Wuhan 430000, Hubei, China.
Open medicine (Warsaw, Poland)
|October 24, 2023
概括
蛋白质S100A4通过促进呼吸道炎症和上皮-介质细胞过渡 (EMT) 来促进喘. 在小鼠模型中,用抗体阻止S100A4可降低喘症状,并预防EMT.
科学领域:
- 肺部医学 肺部医学
- 免疫学 免疫学 免疫学
- 细胞生物学 细胞生物学
背景情况:
- 喘是一种慢性呼吸道疾病,其特点是气道炎症和重塑.
- 表皮介质转换 (EMT) 在喘期间在呼吸道重塑中发挥着重要作用.
- 蛋白质S100A4已涉及到各种炎症和纤维化的过程.
研究的目的:
- 调查S100A4在喘发病过程中的作用,特别是其对呼吸道炎症和EMT的影响.
- 在喘小鼠模型中评估针对S100A4的治疗潜力.
主要方法:
- 在小鼠中使用卵蛋白 (OVA) 敏感化和挑战诱导喘.
- 小鼠接受了抗S100A4抗体或控制IgG的治疗.
- 评估了气道炎症,气道过敏反应和气道改造.
- 通过西式涂抹分析分析了EMT标记物 (维门丁,α-SMA,E-cadherin).
- 在用家用粉尘 (HDM) 刺激的人类支气管上皮细胞中评估了EMT,并用S100A4降低调节治疗.
主要成果:
- 在喘小鼠中,S100A4水平升高.
- 抗S100A4抗体治疗减弱了呼吸道的过敏反应,炎症和重塑.
- 在S100A4抑制下调的EMT标志物 (vimentin,α-SMA) 和上调的E-cadherin.
- 在HDM刺激的人类支气管上皮细胞中降低S100A4抑制EMT.
结论:
- S100A4促进呼吸道炎症和喘中的EMT.
- 用抗体向S100A4是一种潜在的喘治疗策略.
- 抑制S100A4可以通过防止EMT来改善气道重塑.
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