一个LPS诱导炎症模型的RNA-Seq揭示了炎症过程的转录形状模式
Kisung Sheen1,2, Seokho Myung1,3, Dong-Min Lee1,4
1Translational-Transdisciplinary Research Center, Clinical Research Institute, Kyung Hee University College of Medicine, Kyung Hee University Hospital at Gangdong, Seoul 05278, Republic of Korea.
Life (Basel, Switzerland)
|May 25, 2024
概括
脂聚糖 (LPS) 诱导的炎症模型反映了人类疾病,揭示了共享的基因表达模式. 天生的免疫基因增加,而适应性免疫基因减少,突出了炎症中的氧化应激.
科学领域:
- 免疫学 免疫学 免疫学
- 基因组学就是基因组学.
- 系统生物学 系统生物学
背景情况:
- 脂聚糖 (LPS) 诱导炎症模型是研究炎症过程的经济有效和可重复的工具.
- 目前的验证通常依赖于细胞因子标记物,但对基因调节的更深入理解需要更广泛的分析.
- 研究炎症中的基因调节机制需要将已建立的模型与人类疾病转录组进行比较.
研究的目的:
- 严格比较LPS诱导炎症模型的转录特征与表现出全身炎症的人类疾病.
- 评估LPS模型的适用性,以了解各种炎症触发器中的基因调节机制.
- 探索间接相关的炎症反应系统中的基因表达模式,包括综合应激反应 (ISR),氨酸-氨酸-阿尔多斯特系统 (RAAS) 和未折叠蛋白质反应 (UPR).
主要方法:
- 使用了多个全血批量RNA测序 (RNA-seq) 数据集.
- 进行了交叉条件验证,将LPS模型与全身性红斑狼 (SLE) 患者,登革热感染,候选菌感染和黄金杆菌暴露相比较.
- 采用定制的核心炎症基因列表进行全面分析.
主要成果:
- 在LPS模型和人类炎症状况中观察到先天免疫相关基因的高表达和适应性免疫相关基因的抑制表达.
- 确定了与细胞压力和线粒体天生的免疫反应相关的基因的上调.
- 突出了氧化应激作为LPS诱导和其他炎症背景中的核心驱动因素.
结论:
- 由LPS诱导的炎症模型有效地回顾了人类疾病中观察到的系统性炎症的关键转录特征.
- 基因表达分析揭示了各种炎症刺激中先天免疫激活和适应性免疫抑制的共同模式.
- 氧化应激在炎症的病理生理学中发挥着关键作用,正如与压力相关的和线粒体基因的上调调节所表明的那样.
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