由HFD诱导的LPS转位和血脂升高加剧了过敏性鼻炎的炎症反应
Shaopeng Peng1, Xuyang Cai1, Jing Tang1
1Department of Pharmacy, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Scientific reports
|April 15, 2025
概括
高脂肪饮食 (HFD) 通过破坏肠道屏障,增加诸如脂多糖 (LPS) 和脂质等炎症触发物,并激活关键炎症通路,使过敏性鼻炎 (AR) 恶化.
科学领域:
- 免疫学 免疫学 免疫学
- 胃肠病学 胃肠病学
- 营养科学 营养科学
背景情况:
- 过敏性鼻炎 (AR) 是一种广泛的慢性疾病.
- 高脂肪饮食 (HFD) 越来越多地与增加对AR的敏感性有关.
- 了解连接饮食和AR的机制对于公共健康至关重要.
研究的目的:
- 在大鼠模型中研究HFD对卵蛋白 (OVA) 诱导的AR的影响.
- 探索HFD对肠道屏障完整性,全身炎症和关键分子通路的影响.
- 通过体外巨模型验证发现.
主要方法:
- 利用一种对OVA敏感的AR老鼠模型养一个HFD.
- 评估肠道屏障功能 (紧结蛋白),血清脂质和LPS水平,以及炎症标志物 (NLF,血清).
- 在组织中和体外使用用棕酸 (PA) 和LPS治疗的THP-1巨细胞检查NF-κB和NLRP3炎症酶激活.
主要成果:
- 在HFD养的AR大鼠中,紧结蛋白减少,血清脂质和LPS增加,鼻腔和血清样本炎症增加.
- 在HFD养的AR大鼠的鼻腔和结肠组织中,NF-κB和NLRP3炎症酶活性显著增强.
- 在体外,PA和LPS协同扩大了巨细胞的炎症反应,反映了体内发现.
结论:
- 由HFD引起的肠壁功能障碍促进LPS转移到血液中.
- 血清LPS和脂质升高通过NF-κB和NLRP3炎症酶激活加剧AR炎症.
- 针对肠道健康的饮食干预措施可能有利于管理过敏性鼻炎.
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