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简短报告:体外感染伯氏疏螺旋体后巨噬细胞炎症反应及细胞死亡与关节炎抗性的关联

Short report: Association of macrophage inflammatory response and cell death after in vitro Borrelia burgdorferi infection with arthritis resistance.

作者信息

Glickstein Lisa J, Coburn Jenifer L

机构信息

Center for Immunology and Inflammatory Diseases, Massachusetts General Hospital, Boston, Massachusetts 02129, USA.

出版信息

Am J Trop Med Hyg. 2006 Nov;75(5):964-7.

Abstract

Susceptibility to Borrelia burgdorferi infection and subsequent arthritis is genetically determined in mice and determined by innate immunity. Accordingly, macrophage responses to B. burgdorferi challenge may differ between mouse strains. Bone marrow-derived macrophages were infected ex vivo with clonal B. burgdorferi strain N40. Interleukin-12 and tumor necrosis factor-alpha (TNF-alpha) production were higher in macrophages from resistant C57Bl/6 mice than in macrophages from susceptible C3H/HeJ mice. However, TNF-alpha production was observed in lower concentrations in C3H/HeJ (toll-like receptor-4(-/-)) macrophages than in C3H/FeJ (TLR4(+/+)) macrophages, suggesting that TLR4 might contribute to the response to B. burgdorferi. A higher cytokine response to B. burgdorferi was associated with cell death in macrophages from resistant C57Bl/6 mice. Understanding variability in the response of macrophages to B. burgdorferi may contribute to understanding Lyme arthritis.

摘要

小鼠对伯氏疏螺旋体感染及后续关节炎的易感性由基因决定,并由先天免疫决定。因此,不同小鼠品系的巨噬细胞对伯氏疏螺旋体攻击的反应可能不同。用克隆的伯氏疏螺旋体菌株N40对骨髓来源的巨噬细胞进行体外感染。抗性C57Bl/6小鼠的巨噬细胞中白细胞介素-12和肿瘤坏死因子-α(TNF-α)的产生高于易感C3H/HeJ小鼠的巨噬细胞。然而,C3H/HeJ(Toll样受体-4(-/-))巨噬细胞中TNF-α的产生浓度低于C3H/FeJ(TLR4(+/+))巨噬细胞,这表明TLR4可能有助于对伯氏疏螺旋体的反应。对伯氏疏螺旋体更高的细胞因子反应与抗性C57Bl/6小鼠巨噬细胞的细胞死亡有关。了解巨噬细胞对伯氏疏螺旋体反应的变异性可能有助于理解莱姆关节炎。

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