短链脂肪酸调节IPEC-J2细胞对致病性大肠杆菌LPS激活的PBMC的反应
Melania Andrani1, Luca Ferrari1, Paolo Borghetti1
1Department of Veterinary Science, University of Parma, Strada del Taglio 10, 43126 Parma, Italy.
Research in veterinary science
|March 21, 2024
概括
像酸和酸这样的短链脂肪酸 (SCFA) 可以通过减少肠道炎症和氧化应激来帮助猪. 这些有益的化合物支持肠道健康和屏障完整性,即使在致病性大肠杆菌感染期间.
科学领域:
- 动物科学动物科学
- 免疫学 免疫学 免疫学
- 胃肠病学 胃肠病学
背景情况:
- 猪的肠道疾病,特别是年轻动物的肠道疾病,通常是由诸如致病性大肠杆菌等感染引发的,导致营养吸收受损.
- 来自大肠杆菌的脂聚糖 (LPS) 与肠道细胞相互作用,激活免疫反应并可能损害肠道屏障.
- 短链脂肪酸 (SCFA) 以它们对肠道上皮细胞和免疫细胞的有益作用而闻名,这表明它们在减轻肠道炎症方面可能发挥作用.
研究的目的:
- 为了研究酸盐和酸盐对肠上皮细胞 (IPEC-J2) 和由LPS.激活的猪外周血液单核细胞 (PBMCs) 的作用.
- 评估SCFA调节炎症标志物和肠道屏障完整性的能力,在模拟激活免疫状态的共同培养模型中.
主要方法:
- 使用IPEC-J2细胞和LPS (来自大肠杆菌O111:B4) 刺激的猪PBMCs建立了一个共同培养模型.
- 该研究评估了IPEC-J2的活力,氧化的产生,以及先天性和炎症标志物的表达 (BD-1,TLR-4,IL-8,TNF-α,NF-κB,TGF-β).
- 在不同的LPS刺激水平下,分析了乙酸和酸对炎症媒介和紧结蛋白 (claudin-4,zonula occludens-1) 的影响.
主要成果:
- 在LPS刺激下,IPEC-J2活力降低,氧化和炎症标志物表达量增加.
- 乙酸和酸治疗改善了细胞活力,减少了氧化应激,并降低了炎症介质的调节.
- 根据LPS刺激的强度和持续时间,SCFA不同调节紧结蛋白和炎症反应,表明复杂的相互作用.
结论:
- 共同培养模型有效地模拟了炎症期间肠道细胞和激活的免疫细胞之间的相互作用.
- 在猪肠模型中,乙酸和酸显示出对LPS诱导的炎症和屏障破坏的保护作用.
- SCFA对肠道免疫和屏障功能表现出剂量和时间依赖的调节作用,突出了它们在治疗猪肠道疾病方面的治疗潜力.
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