The ability to induce several cytokines relevant to tuberculosis (TNF-α, IL-1β, IL-6, IL-12p40 and IL-23) by cord factor (trehalose dimycolate) from Mycobacterium alvei CR-21(T) and Mycobacterium brumae CR-270(T) was studied in the cell lines RAW 264.7 and THP-1, and compared to the ability of cord factor from Mycobacterium tuberculosis H37Rv, where this glycolipid appears to be implicated in the pathogenesis of tuberculosis. Details of the fine structure of these molecules were obtained by NMR and MS. The mycoloyl residues were identified as α and (ω-1)-methoxy in M. alvei CR-21(T) and α in M. brumae CR-270(T); in both cases they were di-unsaturated instead of cyclopropanated as found in M. tuberculosis. In RAW 264.7 cells, cord factors from M. alvei CR-21(T), M. brumae CR-270(T) and M. tuberculosis differed in their ability to stimulate IL-6, the higher levels corresponding to the cord factor from M. tuberculosis. In THP-1 cells, a similar overall profile of cytokines was found for M. alvei CR-21(T) and M. brumae CR-270(T), with high proportions of IL-1β and TNF-α, and different from M. tuberculosis, where IL-6 and IL-12p40 prevailed. The data obtained indicate that cord factors from the atypical mycobacteria M. alvei CR-21(T) and M. brumae CR-270(T) stimulated the secretion of several pro-inflammatory cytokines, although there were some differences with those of M. tuberculosis H37Rv. This finding seems to be due to their particular mycoloyl substituents and could be of interest when considering the potential adjuvanticity of these molecules.

译文

在细胞系原始264.7和THP-1中研究了脐带因子 (海藻糖二CR-270) 诱导几种与结核病相关的细胞因子 (TNF-α,IL-1β,IL-6,IL-12p40和IL-23) 的能力,与结核分枝杆菌H37Rv的脐带因子的能力相比,该糖脂似乎与结核病的发病机理有关。通过NMR和MS获得了这些分子的精细结构的详细信息。菌酰基残基在CR-21(T) 中被鉴定为 α 和 (ω-1)-甲氧基,而在CR-270(T) 中被鉴定为 α; 在这两种情况下,它们都是二不饱和的,而不是在结核分枝杆菌中发现的环丙烷。在原始264.7细胞中,来自肺泡CR-21(T),布鲁氏菌CR-270(T) 和结核分枝杆菌的脐带因子在刺激IL-6的能力上有所不同,较高水平对应于结核分枝杆菌的脐带因子。在THP-1细胞中,发现肺泡支原体CR-21(T) 和CR-270支原体 (T) 具有相似的细胞因子总体特征,IL-1β 和TNF-α 比例很高,与结核支原体不同,IL-6和IL-12p40盛行。获得的数据表明,来自非典型分枝杆菌CR-21(T) 和布鲁氏菌CR-270(T) 的脐带因子刺激了几种促炎细胞因子的分泌,尽管与结核分枝杆菌H37Rv有一些差异。这一发现似乎是由于它们特定的mycoloyl取代基,并且在考虑这些分子的潜在可调性时可能会引起关注。

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