Vitamin B5 Reduces Bacterial Growth via Regulating Innate Immunity and Adaptive Immunity in Mice Infected with Mycobacterium tuberculosis.
Vitamin B5 Reduces Bacterial Growth via Regulating Innate Immunity and Adaptive Immunity in Mice Infected with Mycobacterium tuberculosis.
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DOI：
10.3389/fimmu.2018.00365
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发表时间：
2018
影响因子：
7.3
通讯作者：
Ma L
中科院分区：
文献类型：
--
作者：
He W;Hu S;Du X;Wen Q;Zhong XP;Zhou X;Zhou C;Xiong W;Gao Y;Zhang S;Wang R;Yang J;Ma L
维生素调节免疫的机制及其作为辅助治疗结核病的作用已逐渐成为重要的研究课题。研究发现，维生素B5 （VB5）可促进上皮细胞表达炎症因子。我们旨在研究VB5在感染结核分枝杆菌H37Rv的巨噬细胞中的促炎和抗菌作用，以及VB5在体内治疗结核病的潜力。我们通过研究VB5刺激感染h37rv的巨噬细胞炎症信号分子NF-κB、AKT、JNK、ERK、p38的激活、两种主要炎症因子（肿瘤坏死因子和白细胞介素-6）的表达和细菌负荷，探讨VB5对巨噬细胞炎症和抗菌反应的影响。我们进一步用VB5处理感染H37Rv的小鼠，探讨VB5促进H37Rv在肺中的清除和VB5调节炎症细胞百分比的作用。我们的数据显示，VB5增强了感染H37Rv的巨噬细胞的吞噬和炎症反应。在感染后1、2和4周，口服VB5可减少小鼠肺部H37Rv菌落形成单位的数量。此外，VB5调节巨噬细胞百分比，促进CD4+ T细胞表达干扰素-γ和白细胞介素-17；然而，对多形核中性粒细胞、CD4+和CD8+ T细胞的百分比没有影响。综上所述，VB5通过调节先天免疫和适应性免疫来抑制MTB的生长。
The mechanisms by which vitamins regulate immunity and their effect as an adjuvant treatment for tuberculosis have gradually become very important research topics. Studies have found that vitamin B5 (VB5) can promote epithelial cells to express inflammatory cytokines. We aimed to examine the proinflammatory and antibacterial effect of VB5 in macrophages infected with Mycobacterium tuberculosis (MTB) strain H37Rv and the therapeutic potential of VB5 in vivo with tuberculosis. We investigated the activation of inflammatory signal molecules (NF-κB, AKT, JNK, ERK, and p38), the expression of two primary inflammatory cytokines (tumor necrosis factor and interleukin-6) and the bacterial burdens in H37Rv-infected macrophages stimulated with VB5 to explore the effect of VB5 on the inflammatory and antibacterial responses of macrophages. We further treated the H37Rv-infected mice with VB5 to explore VB5’s promotion of the clearance of H37Rv in the lungs and the effect of VB5 on regulating the percentage of inflammatory cells. Our data showed that VB5 enhanced the phagocytosis and inflammatory response in macrophages infected with H37Rv. Oral administration of VB5 decreased the number of colony-forming units of H37Rv in lungs of mice at 1, 2, and 4 weeks after infection. In addition, VB5 regulated the percentage of macrophages and promoted CD4+ T cells to express interferon-γ and interleukin-17; however, it had no effect on the percentage of polymorphonuclear neutrophils, CD4+ and CD8+ T cells. In conclusion, VB5 significantly inhibits the growth of MTB by regulating innate immunity and adaptive immunity.
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影响因子：
11.1
作者：
Hu S;He W;Du X;Yang J;Wen Q;Zhong XP;Ma L
通讯作者：
Ma L
DOI：
10.4049/jimmunol.1000866
发表时间：
2010-07-15
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Rajaram MV;Brooks MN;Morris JD;Torrelles JB;Azad AK;Schlesinger LS
通讯作者：
Schlesinger LS
影响因子：
64.8
作者：
Kimmey JM;Huynh JP;Weiss LA;Park S;Kambal A;Debnath J;Virgin HW;Stallings CL
通讯作者：
Stallings CL
影响因子：
3.4
作者：
Lerner TR;Borel S;Gutierrez MG
通讯作者：
Gutierrez MG
影响因子：
--
作者：
Eldridge, Alison L.
通讯作者：
Eldridge, Alison L.