Vitamin A deficiency exacerbates murine lyme arthritis
Vitamin A deficiency exacerbates murine lyme arthritis
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DOI：
10.1093/infdis/174.4.747
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发表时间：
1996-10-01
影响因子：
6.4
通讯作者：
Hayes, CE
中科院分区：
文献类型：
--
作者：
Cantorna, MT;Hayes, CE
维生素A缺乏使宿主易于产生强烈的炎症反应，这表明它可能会促进对疾病的易感性，如莱姆关节炎，其中活化的巨噬细胞和炎性细胞因子的产生是致病的。受感染的小鼠血清视黄醇迅速下降，这与关节炎的发作有关。视黄醇含量最低的小鼠比视黄醇含量最高的小鼠更早、更严重地患上急性关节炎。与对照组相比，伯氏疏螺旋体感染的维生素A缺乏小鼠中发现了更早和更强的白细胞介素（IL）-12，干扰素-γ（IFN）-γ和肿瘤坏死因子反应。螺旋体诱导IFN-γ从未引发的细胞分泌，和类维生素A在体外抑制IFN-γ的合成。维生素A缺乏可通过增强由螺旋体驱动的IFN-γ分泌引发的急性致关节炎性反应而加重急性莱姆关节炎。相反，维生素A可以通过阻断IFN-γ和IL-12的合成来减轻急性莱姆关节炎的病理。
Vitamin A deficiency predisposes the host for a strong inflammatory response, suggesting that it may foster susceptibility to diseases, such as Lyme arthritis, in which activated macrophage and inflammatory cytokine production are pathogenic. Infected mice had a rapid serum retinol decline that correlated with the onset of arthritis. The mice with the least retinol developed acute arthritis earlier and more severely than those with the highest retinol. Earlier and stronger interleukin (IL)-12, interferon-gamma (IFN)-gamma, and tumor necrosis factor responses were found in Borrelia burgdolferi-infected, vitamin A-deficient mice compared with controls. The spirochetes induced IFN-gamma secretion from unprimed cells, and retinoid addition in vitro inhibited IFN-gamma synthesis. Vitamin A deficiency may exacerbate acute Lyme arthritis by enhancing an acute arthritogenic inflammatory response initiated by spirochete-driven IFN-gamma secretion. Conversely, vitamin A may lessen acute Lyme arthritis pathology by blocking IFN-gamma and IL-12 synthesis.