老龄化,来自大脑的神经营养因子和过敏原诱导的小鼠肺部反应
Li Y Drake1, Benjamin B Roos1, Sarah A Wicher1
1Department of Anesthesiology and Perioperative Medicine, Mayo Clinic, Rochester, Minnesota, United States.
概括
在患有喘的小鼠中,衰老导致肺部反应能力降低,但呼吸道重塑和衰老增加. 呼吸道光滑肌中的脑衍生神经营养因子 (BDNF) 影响这些与年龄相关的变化,这表明衰老途径有助于老年人喘.
科学领域:
- 肺部医学 肺部医学
- 衰老研究研究 衰老研究
- 免疫学 免疫学 免疫学
背景情况:
- 老年人的喘呈现出严重程度和发病率的增加.
- 呼吸道光滑肌肉通过过度反应和重塑在喘病因发生中发挥着关键作用.
- 气道结构和功能的与衰老相关的变化,包括衰老,可能会影响老年人的喘.
研究的目的:
- 在过敏性喘的小鼠模型中调查衰老对呼吸道过敏反应,结构重塑,炎症和衰老的影响.
- 确定脑衍生神经营养因子 (BDNF) 在光滑肌肉中对与年龄相关的喘病理学的作用.
主要方法:
- 不同年龄 (4,18,24个月) 的野生型和光滑肌特异性BDNF淘汰小鼠暴露于混合过敏原.
- 使用 flexiVent 评估肺功能,并分析肺组织学.
- 测量了炎症,细胞因子,化学因子和衰老标志物 (p21,-p53,-γH2A.X).
主要成果:
- 与年轻小鼠相比,老年小鼠 (18个月和24个月) 的呼吸道阻力降低,服从性增加.
- 在老年小鼠中消除光滑肌肉BDNF减弱的呼吸道过敏反应.
- 衰老导致支气管厚度增加,肺炎减少,过敏原诱导的细胞因子/化学因子表达减少.
- 在老老鼠的呼吸道中,衰老标志物增加.
结论:
- 老龄化改变了对过敏原的呼吸道反应,其特点是炎症减少,但呼吸道重塑和衰老增加.
- 从光滑肌肉中获得的BDNF在老年喘小鼠中调节气道过敏反应方面发挥着作用.
- 气道衰老,与过敏原暴露相结合,可能是老年人喘病原的一个重要因素.
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