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Vivek P Varma^1,2, Ramudu Bankala¹, Ajay Kumar^1,3

¹Laboratory of Vaccine Immunology, National Institute of Animal Biotechnology, Hyderabad 500032, India.

|November 7, 2023

概括

莱普托斯皮拉脂聚糖 (LPS) 在不同的宿主中引发各种先天性免疫反应,与大肠杆菌LPS不同. 这项研究揭示了宏细胞活动和细胞因子生产的血清细胞特异调节.

科学领域:

传染性疾病传染性疾病
免疫学免疫学免疫学
微生物学微生物学

背景情况:

牛螺旋病是一种全球性动物性疾病,由致病性Leptospira spp.引起. 有超过300个伺服器.
脂多糖 (LPS) 是莱普托斯皮拉的一个关键抗原,影响血清细胞的特异性和宿主反应.
众所周知,LeptoSpira LPS的内毒性低于其他细菌LPS,但其差异性免疫调节能力尚不清楚.

研究的目的:

为了研究由LPS从各种Leptospira血清病毒中引起的差异性先天免疫反应.
为了比较Leptospira LPS (L-LPS) 在来自耐药 (小鼠) 和易感 (人类,牛) 主体的巨细胞中的免疫调节作用.
阐明L-LPS诱导的信号通路和细胞反应.

主要方法:

从三种致病性Leptospira血清和一种非致病性菌株净化LPS.
在小鼠,人类和牛的巨细胞中测试L-LPS免疫调节能力.
对托尔类受体 (TLR) 的依赖性,MyD88适配器参与和MAP激酶通路 (p38,ERK) 的分析.
评估巨细胞化,炎症酶激活 (IL-1β产生) 和亡 (TNF,NO介导).

主要成果:

L-LPS诱导了差异性前炎性反应:在小鼠巨细胞中更高,在人类和牛巨细胞中更低,总体而言,免疫刺激能力低于大肠杆菌LPS.
人类巨细胞的反应是TLR2依赖的,而小鼠的反应是TLR4依赖/CD14独立的.
由L-LPS激活的巨细胞显示Leptospira的细胞增强,特别是当用血清匹配的LPS刺激时.
L-LPS激活了规范性和非规范性炎症体,产生了 IL-1β 无需灭,并诱导了早期 (TNF) 和晚期 (NO) 灭.

结论:

与大肠杆菌LPS相比,Leptospira LPS引起了独特和差异化的先天免疫反应,受到血清菌和宿主物种的影响.
L-LPS的非典型性质和结构差异有助于其独特的免疫调节特性.
了解这些差异性反应对于开发针对性治疗和乳螺旋病疫苗至关重要.

关键词:

莱普托斯皮拉 (Leptospira) 是一个类动物.灭症 (apoptosis) 是一种死亡的过程.一些炎症一些炎症这是先天的反应.脂多糖类糖化物 (Lipopolysaccharide) 是一种脂多糖类糖.

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