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1,25(OH)D 治疗改变了结核分枝杆菌感染小鼠的肉芽肿反应。

1,25 (OH)D treatment alters the granulomatous response in M. tuberculosis infected mice.

机构信息

Department of Medicine, Center for Emerging Pathogens, Rutgers, New Jersey Medical School, Newark, NJ, USA.

Department of Microbiology, Biochemistry and Molecular Genetics, Rutgers, New Jersey Medical School, Newark, New Jersey, USA.

出版信息

Sci Rep. 2016 Oct 4;6:34469. doi: 10.1038/srep34469.

DOI:10.1038/srep34469
PMID:27698450
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5048147/
Abstract

Induction of cathelicidin-mediated antimicrobial pathway against intracellular M. tuberculosis by 1,25-dihydroxyvitamin D (1,25(OH)D), the active form of vitamin D, has been documented in vitro. However, in in vivo studies related to inflammatory disorders, 1,25(OH)D has been demonstrated to induce an anti-inflammatory response. We therefore examined whether in the murine model of tuberculosis, the anti-inflammatory effects of 1,25(OH)D would affect the outcome of M. tuberculosis infection. We show here that administration of 1,25(OH)D to M. tuberculosis infected mice led to a change in lung granuloma architecture, characterized by a marked decrease in B cell lymphocytic aggregates. Consistent with the altered granulomas, 1,25(OH)D-treated mice also exhibited significantly higher bacterial burden in the lungs compared to the control group. These findings highlight the need to further investigate the effect of vitamin D on host immunity to M. tuberculosis in the context of the granulomatous response.

摘要

1,25-二羟维生素 D(1,25(OH)D),维生素 D 的活性形式,已被证明可在体外诱导抗菌肽介导的抗分枝杆菌途径。然而,在与炎症性疾病相关的体内研究中,1,25(OH)D 已被证明可诱导抗炎反应。因此,我们研究了在结核分枝杆菌感染的小鼠模型中,1,25(OH)D 的抗炎作用是否会影响结核分枝杆菌感染的结果。我们在这里显示,给予感染结核分枝杆菌的小鼠 1,25(OH)D 治疗导致肺肉芽肿结构发生变化,特征为 B 细胞淋巴细胞聚集明显减少。与改变的肉芽肿一致,与对照组相比,1,25(OH)D 治疗的小鼠肺部的细菌负荷也显著更高。这些发现强调了需要进一步研究维生素 D 在宿主对结核分枝杆菌的免疫反应背景下对肉芽肿反应的影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dca6/5048147/bc129c45d192/srep34469-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dca6/5048147/0d122a839028/srep34469-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dca6/5048147/813e5283e606/srep34469-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dca6/5048147/1922dd017988/srep34469-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dca6/5048147/0d4e8214f743/srep34469-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dca6/5048147/bc129c45d192/srep34469-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dca6/5048147/0d122a839028/srep34469-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dca6/5048147/813e5283e606/srep34469-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dca6/5048147/1922dd017988/srep34469-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dca6/5048147/0d4e8214f743/srep34469-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dca6/5048147/bc129c45d192/srep34469-f5.jpg

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Vitamin D: Metabolism, Molecular Mechanism of Action, and Pleiotropic Effects.
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Pathog Dis. 2019 Jun 1;77(4). doi: 10.1093/femspd/ftz037.
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