Histopathological study on developmental mechanism of the coronary, artery destruction in acute stage Kawasaki Disease patients

川崎病急性期冠状动脉破坏发育机制的组织病理学研究

• 批准号: 14570168
• 负责人: TAKAHASHI Kei
• 金额: $ 1.54万
• 依托单位: Toho University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2002
• 资助国家: 日本
• 起止时间: 2002 至 2003
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-14570168/
• 关键词: Kawasaki disease; Coronary arteritis; Coronary artery aneurysm; Immunoglobulin; Neutrophils; Immunohistochemistry; Systemic vasculitis; Plasma cells; Chlamydia pneumoniae; 形質細胞; 好中球エラスターゼ; マトリクスメタロプロテナーゼ

There has been no morphological evidence that neutrophils infiltrate the coronary arterialn lesions of acute Kawasaki Disease(KD) patients, although clinical data indicate the activation of neutrophils in the peripheral blood. Therefore, we carried out histological examination about the role of neutrophils in the damage to coronary arteries in acute stage of KD. The materials consisted of eight autopsy patients who died during the acute phase of KD. The tissues were fixed and embedded in paraffin. Hematoxylin and eosin, elastica van Gieson and azan-Mallory stainings were performed for routine histological examination. In addition, antibodies to CD3, CD20, CD68, neutrophil elastase and immunoglobulins were used for immunohistochemistry to identify infiltrating cells in the arterial lesions. The inflammatory cells which appeared in the coronary arterial lesions were mainly composed of macrophages in all patients. In addition, numerous neutrophils were also identified in the coronary arterial lesions of the patients who died 10 days after the onset of KD. Neutrophilic infiltration reached a peak earlier than the peaks of CD68+ macrophages, CD3+ lymphocytes and CD20+ lymphocytes. These results suggest that neutrophils are involved in the damage occurring to coronary arteries in the early stage of KD. Vascular dilatation might occur as a result of damage to vascular walls caused by neutrophils, as well as macrophages. We compared histology of coronary arterial lesions between a patient with IVGG administration and a patient without IVGG. It showed the tendency that the degree of CD20+ lymphocytic infiltration was higher in the latter patient. However, there was not difference in plasma cells, CD68+ cells and neutrophils between two patients.

没有形态学的证据表明中性粒细胞浸润急性川崎疾病（KD）患者的冠状动脉病变，尽管临床数据表明外周血中嗜中性粒细胞的激活。因此，我们对中性粒细胞在KD急性阶段损害冠状动脉损害中的作用进行了组织学检查。这些材料由八名尸检患者组成，他们在KD的急性期死亡。固定组织并嵌入石蜡中。进行苏木精和曙红，弹性弹性，弹性蛋白和阿赞彩色染色进行常规组织学检查。此外，使用CD3，CD20，CD68，中性粒细胞弹性酶和免疫球蛋白的抗体用于免疫组织化学，以鉴定动脉病变中的浸润细胞。出现在冠状动脉病变中的炎症细胞主要由所有患者的巨噬细胞组成。此外，在KD发作后10天死亡的患者的冠状动脉病变中也发现了许多嗜中性粒细胞。中性粒细胞浸润比CD68+巨噬细胞，CD3+淋巴细胞和CD20+淋巴细胞的峰早。这些结果表明，嗜中性粒细胞参与KD早期冠状动脉造成的损害。血管扩张可能是由于中性粒细胞以及巨噬细胞引起的血管壁的损害而发生的。我们比较了IVGG给药患者与无IVGG患者之间的冠状动脉病变的组织学。它表明，后一患者的CD20+淋巴细胞浸润程度更高。但是，两名患者之间的浆细胞，CD68+细胞和中性粒细胞没有差异。

项目成果

高橋 啓, 大原関利章, 他: "川崎病既往は粥状動脈硬化症の危険因子となりえるか(病理の立場より)"小児内科. 35. 1435-1346 (2003)

Kei Takahashi、Toshiaki Oharaseki 等人：“川崎病病史是否是动脉粥样硬化的危险因素（从病理学角度来看）” 35. 1435-1346 (2003)

K.Takahashi, et al.: "Histopathological features of murine systemic vasculitis caused by Candida albicans extract-an animal model of Kawasaki Disease"Inflammation Research. 53. 72-77 (2004)

K.Takahashi等：“白色念珠菌提取物引起的小鼠系统性血管炎的组织病理学特征——川崎病动物模型”炎症研究。

Takahashi Kei, et al.: "Histopathological features of murine systemic vasculitis caused by Candida albicans extract -an animal model of Kawasaki Disease."Inflammation Research. 53. 72-77 (2004)

Takahashi Kei 等人：“白色念珠菌提取物引起的小鼠系统性血管炎的组织病理学特征 - 川崎病的动物模型。”炎症研究。

高橋 啓: "瘤を確認できなかつた冠状動脈の狭窄性病変への進展の可能性について"Prog.Med.. 22. 1676-1678 (2002)

Kei Takahashi：“无法确认动脉瘤的冠状动脉狭窄病变的可能性”Prog.Med.. 22. 1676-1678 (2002)

高橋 啓: "小児血管炎の病理"病理と臨床. 21. 926-927 (2003)

Kei Takahashi：“小儿血管炎的病理学”病理学和临床实践 21. 926-927 (2003)。