Phosphatidylinositol mannosides: Synthesis and suppression of allergic airway disease
Phosphatidylinositol mannosides: Synthesis and suppression of allergic airway disease
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DOI：
10.1016/j.bmc.2006.04.037
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发表时间：
2006-08-15
影响因子：
3.5
通讯作者：
Harper, Jacquie L.
中科院分区：
文献类型：
--
作者：
Ainge, Gary D.;Hudson, Jennifer;Harper, Jacquie L.
从分枝杆菌中提取的磷脂酰肌醇甘露糖（PIM）先前已被证明可以抑制小鼠的过敏性气道炎症。为了帮助确定活性的结构要求，我们合成了PIM1(2)(1)、PIM1(6)(2)和PIM2(3)，并在过敏性哮喘小鼠模型中测试了它们抑制细胞炎症的能力。合成pim均能有效抑制哮喘模型气道嗜酸性粒细胞增多，其中以PIM16效果最好。观察到所有炎症细胞的抑制，表明细胞炎症的普遍阻断。非甘露糖基化磷脂酰肌醇（PI）没有抑制作用，表明至少有一个α - d -甘露糖基残基是维持活性所必需的。这三种PIM化合物的抑制作用表明，这组化合物的其他成员可能在治疗一系列由炎症细胞浸润引起的疾病中具有价值。(c) 2006 Elsevier Ltd.版权所有。
Phosphatidylinositol mannoside (PIM) extracts from mycobacteria have been shown previously to suppress allergic airway inflammation in mice. To help determine the structural requirements for activity, PIM1(2) (1), PIM1(6) (2) and PIM2 (3) were synthesized and tested for their ability to suppress cellular inflammation in a mouse model of allergic asthma. The synthetic PIMs were all effective in suppressing airway eosinophilia in the asthma model, with PIM16 being the most effective. Suppression of all inflammatory cells monitored was observed, indicating a general blockade of cellular inflammation. Non-mannosylated phosphatidylinositol (PI) had no suppressive effect, indicating that at least one alpha-D-mannopyranosyl residue is necessary for activity. The suppressive effect of the three PIM compounds indicates that other members of this set may be of value in treatment of a range of diseases driven by infiltration of inflammatory cells. (c) 2006 Elsevier Ltd. All rights reserved.