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IL-33和IL-35的相互作用调节了香烟烟雾暴露的Th2/Th17反应,导致HDM诱导的喘
Jing Liu1, Beiting Su1, Peizhi Tao1
1Department of Pulmonary and Critical Care Medicine, The Third Affiliated Hospital of Sun Yat-sen University, Institute of Respiratory Diseases of Sun Yat-sen University, Guangzhou, People's Republic of China.
香烟烟雾通过增加IL-33和减少IL-35加剧喘. 用CpG-ODNs调节这些细胞因子为过敏呼吸道炎症提供了潜在的治疗策略.
科学领域:
- 免疫学 免疫学 免疫学
- 呼吸系统医学 呼吸系统医学
- 分子生物学分子生物学
背景情况:
- 暴露于香烟烟雾 (CS) 是喘发展和恶化的重要危险因素.
- 在CS诱导的喘病原体中,互白素-33 (IL-33) 和互白素-35 (IL-35) 的作用尚不完全理解.
研究的目的:
- 研究CS加剧喘的机制,重点关注IL-33和IL-35之间的相互作用.
- 评估调节IL-33和IL-35水平在CS暴露喘的小鼠模型中的治疗潜力.
主要方法:
- 利用CS暴露喘的小鼠模型,使用IL-33淘汰 (IL-33KO) 和腺病毒介导的IL-35 (Ad-IL-35) 基因转移.
- 在共同培养系统中研究了树突细胞 (DC) 和T辅助者2 (Th2) /T辅助者17 (Th17) 细胞的调节.
- 评估了CpG-oligodeoxynucleotides (CpG-ODNs) 对IL-33和IL-35平衡以及下游信号通路的影响.
主要成果:
- 在喘小鼠中,CS和室内灰尘虫 (HDM) 暴露增加了IL-33和降低了IL-35水平.
- 治疗IL-33 KO或Ad-IL-35显著降低了呼吸道过度反应,杯状细胞增生,呼吸道重塑和炎症细胞透.
- CpG-ODN抑制IL-33/ST2表达和提高IL-35水平,主要来自调节性T细胞 (Tregs),通过抑制树突细胞激活来缓解Th2/Th17炎症.
结论:
- 在CS暴露的喘中,IL-33/ST2通路促进DC-Th2和Th17反应,而IL-35则具有相反的效果.
- 使用CpG-ODN调节IL-33/IL-35平衡,为抑制喘中的过敏气道炎症提供了一个有希望的治疗策略.
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