Allicin enhances host pro-inflammatory immune responses and protects against acute murine malaria infection.
Allicin enhances host pro-inflammatory immune responses and protects against acute murine malaria infection.
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DOI：
10.1186/1475-2875-11-268
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发表时间：
2012-08-08
期刊：
影响因子：
3
通讯作者：
Cao Y
中科院分区：
文献类型：
--
作者：
Feng Y;Zhu X;Wang Q;Jiang Y;Shang H;Cui L;Cao Y
在疟疾感染过程中，多种促炎介质包括IFN-γ、TNF和一氧化氮（NO）在抗寄生虫的保护中起着至关重要的作用。调节宿主免疫是改善疟疾感染结局的重要策略。大蒜素是大蒜的主要生物活性成分，具有抗菌活性。大蒜素还对原生动物寄生虫具有活性，包括疟原虫，其被认为是通过抑制半胱氨酸蛋白酶介导的。在这项研究中，大蒜素的免疫调节活性进行了评估，在急性疟疾感染使用啮齿动物疟疾模型约氏疟原虫17 XL。为了确定大蒜素是否调节针对疟疾感染的宿主免疫应答，在感染约氏疟原虫17 XL后用大蒜素处理小鼠。每天检查死亡率，每隔一天测定寄生虫血症。促炎介质和IL-4通过ELISA定量，而NO水平通过Griess方法测定。流式细胞术检测树突状细胞（DC）、巨噬细胞、CD 4 + T细胞和调节性T细胞（Treg）的数量。大蒜素以剂量依赖性方式减少寄生虫血症并延长宿主的存活时间。这种效果至少部分是由于宿主免疫应答的改善。结果表明，大蒜素处理组小鼠外周血中IFN-γ、TNF、IL-12 p70和NO等促炎介质的产生明显增加，CD 4 + T细胞、DC和巨噬细胞的绝对数量明显增加。此外，大蒜素促进了CD 11 c + DCs的成熟，而它没有引起IL-4和抗炎细胞因子IL-10水平的重大变化。大蒜素可通过增强宿主的天然免疫和适应性免疫应答，部分保护宿主抵抗约氏疟原虫17 XL。
During malaria infection, multiple pro-inflammatory mediators including IFN-γ, TNF and nitric oxide (NO) play a crucial role in the protection against the parasites. Modulation of host immunity is an important strategy to improve the outcome of malaria infection. Allicin is the major biologically active component of garlic and shows anti-microbial activity. Allicin is also active against protozoan parasites including Plasmodium, which is thought to be mediated by inhibiting cysteine proteases. In this study, the immunomodulatory activities of allicin were assessed during acute malaria infection using a rodent malaria model Plasmodium yoelii 17XL. To determine whether allicin modulates host immune responses against malaria infection, mice were treated with allicin after infection with P. yoelii 17XL. Mortality was checked daily and parasitaemia was determined every other day. Pro-inflammatory mediators and IL-4 were quantified by ELISA, while NO level was determined by the Griess method. The populations of dendritic cells (DCs), macrophages, CD4+ T and regulatory T cells (Treg) were assessed by FACS. Allicin reduced parasitaemia and prolonged survival of the host in a dose-dependent manner. This effect is at least partially due to improved host immune responses. Results showed that allicin treatment enhanced the production of pro-inflammatory mediators such as IFN-γ, TNF, IL-12p70 and NO. The absolute numbers of CD4+ T cells, DCs and macrophages were significantly higher in allicin-treated mice. In addition, allicin promoted the maturation of CD11c+ DCs, whereas it did not cause major changes in IL-4 and the level of anti-inflammatory cytokine IL-10. Allicin could partially protect host against P. yoelii 17XL through enhancement of the host innate and adaptive immune responses.
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