Analysis of a murine nickel-allergy model promoted by endotoxin

内毒素促进的小鼠镍过敏模型分析

• 批准号: 18591995
• 负责人: ENDO Yasuo
• 金额: $ 2.41万
• 依托单位: Tohoku University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2006
• 资助国家: 日本
• 起止时间: 2006 至 2007
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-18591995/
• 关键词: Metal allergy; Nickel allergy; Innate Immunity; Histamine; IL-1; Lipopolysaccharide; Macrophages; Mast cells; lipopolysaccharide; 好塩基球; T細胞

2006: We found that endotoxin from gram-negative bacteria (or lipopolysaccharide, LPS) strongly promotes nickel (Ni)-allergy in the steps of both sensitization and elicitation, and we clarified the followings (published in Clin Exp Allergy 2007;37:743-751).1. Inflammation was severer in Th1-dominant mice than in Th2-dominant mice.2. Extent of inflammation in mice deficient in TNF or T cells was similar to that in control mice, while it was markedly weak in IL-1-deficient mice and in macrophage-depleted mice.3. The activity of histamine-forming enzyme (HDC) increased in parallel with the progress of inflammation.4. Inflammation tended to be augmented in mast cell-deficient mice, but markedly weak in HDC-deficient mice.5. LPS also promoted the establishment of allergies to other metals (Cr, Co, Pd, Cu, and Ag).2007: We found the followings (will be submitted after additional experiments)1. In addition to macrophages, NK and/or basophiles may be involved in the development of Ni-allergy.2. Ni-sensitized mice responded to Cr, Co, Pd, Cu, and Ag, too.3. Histamine was involved in the process of elicitation.4. In addition to LPS, other bacterial constituents or related inflammatory substances (MDP, mannan, polyI:polyC, or TLR2 ligands, concanavalin A, nitrogen-containing bisphosphonates) also promoted Ni-allergy in the steps of both sensitization and elicitation.5. In the elicitation step, Ni, under the presence of LPS, induced inflammation at so low concentration as 1x10^<-12> M (i.e., inflammation may dramatically enhances the sensitivity to metal allergies).

2006年：我们发现革兰氏阴性细菌(或脂多糖)的内毒素在致敏和诱导两个步骤中都强烈促进镍(Ni)过敏，我们澄清了以下内容(发表在Clin Exp过敏2007；37：743-751)。Th1显性小鼠的炎症反应比Th2显性小鼠严重。肿瘤坏死因子或T细胞缺陷小鼠的炎症程度与对照组相似，而IL-1缺陷小鼠和巨噬细胞耗竭小鼠的炎症程度明显较弱。组胺形成酶(HDC)活性随炎症进展而升高。肥大细胞缺陷小鼠的炎症反应倾向于增强，但HDC缺陷小鼠的炎症反应明显较弱。脂多糖还促进了对其他金属(铬、钴、钯、铜和银)的过敏。2007：我们发现以下内容(将在额外的实验后提交)1.除巨噬细胞外，NK和/或嗜碱性细胞可能参与了镍过敏的发生。镍致敏小鼠对铬、钴、钯、铜和银也有反应。组胺参与了兴奋过程。除内毒素外，其他细菌成分或相关炎性物质(MDP、甘露聚糖、PolyI：PolyC或TLR2配体、刀豆蛋白A、含氮双膦酸盐)也通过敏化和激发两个步骤促进镍过敏。在诱导步骤中，镍在脂多糖存在下，在低浓度(1×10^-12；gt；M)下诱导炎症(即炎症可显著增强对金属过敏的敏感性)。

项目成果

Ni(+LPS)感作マウスでのNiと他金属との交差allergy反応

Ni(+LPS)致敏小鼠中Ni与其他金属的交叉过敏反应

• 发表时间: 2006
• 作者: 金原正敬;佐藤直毅;黒石智誠;菅原俊二;遠藤康男
• 通讯作者: 遠藤康男

自然免疫によるNiアレルギーの誘導

先天免疫诱导镍过敏

• 发表时间: 2006
• 作者: 佐藤直毅;金原正敬;黒石智誠;岩倉洋一郎;菅原俊二;遠藤康男
• 通讯作者: 遠藤康男

マウスにおける金属アレルギー:LPSによる増強と交差反応

小鼠金属过敏：LPS 的增强和交叉反应

• 发表时间: 2006
• 作者: 金原正敬;佐藤直毅;黒石智誠;菅原俊二;遠藤康男
• 通讯作者: 遠藤康男

LPSは自然免疫およびヒスタミン合成酵素histidine decarboxylaseを介して金属アレルギーを促進する

LPS 通过先天免疫和组胺合成酶组氨酸脱羧酶促进金属过敏

• 发表时间: 2006
• 作者: 佐藤直毅;金原正敬;黒石智誠;木村幸平;菅原俊二;遠藤康男
• 通讯作者: 遠藤康男

Lipopolysaccharide promotes and augments metal allergies in mice, dependent on innate immunity and histidine decarboxylase

• DOI: 10.1111/j.1365-2222.2007.02705.x
• 发表时间: 2007-05-01
• 期刊: CLINICAL AND EXPERIMENTAL ALLERGY
• 影响因子: 6.1
• 作者: Sato, N.;Kinbara, M.;Endo, Y.
• 通讯作者: Endo, Y.