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首页> 外文期刊>Clinical & developmental immunology. >Role of Toll-Like Receptor 4 on Lupus Lung Injury and Atherosclerosis in LPS-Challenge ApoE ?/? Mice
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Role of Toll-Like Receptor 4 on Lupus Lung Injury and Atherosclerosis in LPS-Challenge ApoE ?/? Mice

机译：Toll样受体4在LPS挑战ApoE ？/？小鼠中对狼疮肺损伤和动脉粥样硬化的作用

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To investigate the pathologic mechanisms of toll-like receptor 4 (TLR4) in lung injury and atherosclerosis, ApoE~(?/?)or wild-type mice were intraperitoneally administered saline, lipopolysaccharides (LPS), or LPS plus TAK-242 (TLR4 inhibitor), respectively, twice a week for 4 weeks. Serum autoantibody of antinuclear antibody (ANA), anti-double-stranded DNA (anti-dsDNA), and cytokines of interferon-gamma (IFN- γ ), tumor necrosis factor (TNF- α ), and interleukin-1 (IL-1 β ) were assessed by ELISA. Hematoxylin and eosin (HE) and Perl's stains for lung pathomorphology as well as HE staining for atherosclerosis were employed. TLR4 in macrophages was detected by double immunofluorescent staining. While protein expressions of TLR4, nuclear factor-kappa B p65 (NF- κ B p65), and B cell activating factor belonging to the TNF family (BAFF) were examined by immunohistochemistry. We found that serum autoantibody (ANA and anti-dsDNA), cytokines (IFN- γ , TNF- α , IL-1 β ), lung inflammation, and intima-media thickness in brachiocephalic artery were obviously increased after LPS challenge in both genotypes, but to a lesser extent in wild-type strains. And those alterations were alleviated by coadministration of LPS and TAK-242. Mechanistically, upregulation of TLR4, NF- κ b, and BAFF was involved. We concluded that TLR4/NF- κ b/BAFF in macrophages might be a possible common autoimmune pathway that caused lung injury and atherosclerosis. TLR4 signal will be a therapeutic target in atherosclerosis and immune-mediated lung injury.
机译：为了研究Toll样受体4（TLR4）在肺损伤和动脉粥样硬化中的病理机制，对ApoE〜（？/？）或野生型小鼠腹膜内给予生理盐水，脂多糖（LPS）或LPS加TAK-242（TLR4）抑制剂），每周两次，共4周。抗核抗体（ANA），抗双链DNA（anti-dsDNA）的血清自身抗体以及干扰素-γ（IFN-γ），肿瘤坏死因子（TNF-α）和白介素-1（IL-1）的细胞因子通过ELISA评估β）。使用苏木精和曙红（HE）以及用于肺病理形态学的Perl染色以及用于动脉粥样硬化的HE染色。通过双重免疫荧光染色检测巨噬细胞中的TLR4。通过免疫组织化学检查TLR4，核因子κBp65（NF-κBp65）和属于TNF家族（BAFF）的B细胞活化因子的蛋白表达。我们发现两种基因型均受到LPS攻击后，头颅动脉的血清自身抗体（ANA和抗dsDNA），细胞因子（IFN-γ，TNF-α，IL-1β），肺部炎症和内膜中层厚度明显增加，但在野生型菌株中程度较小。 LPS和TAK-242并用可以缓解这些改变。从机理上讲，涉及TLR4，NF-κb和BAFF的上调。我们得出结论，巨噬细胞中的TLR4 /NF-κb/ BAFF可能是引起肺损伤和动脉粥样硬化的一种常见的自身免疫途径。 TLR4信号将成为动脉粥样硬化和免疫介导的肺损伤的治疗靶标。

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