Neutrophilic involvement in the damage to coronary arteries in acute stage of Kawasaki disease
Neutrophilic involvement in the damage to coronary arteries in acute stage of Kawasaki disease
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DOI：
10.1111/j.1442-200x.2005.02049.x
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发表时间：
2005-06-01
影响因子：
1.4
通讯作者：
Yokouchi, Y
中科院分区：
文献类型：
--
作者：
Takahashi, K;Oharaseki, T;Yokouchi, Y
背景：尽管临床数据表明多形核白细胞（PMNL）被激活，但尚无形态学证据表明多形核白细胞（PMNL）浸润急性川崎病（KD）患者的冠状动脉病变。方法：实验材料由8名在川崎病急性期死亡的尸检患者组成。病程从6天到32天不等。将组织固定并包埋在石蜡中。进行苏木精和伊红、elastica van Gieson 和 azan-Mallory 染色以进行常规组织学检查。另外，应用CD3、CD20、CD68和中性粒细胞弹性蛋白酶抗体进行免疫组化，以鉴定动脉病变中的浸润细胞。结果：所有患者冠状动脉病变中出现的炎症细胞主要由巨噬细胞组成。此外，在川崎病发病10天后死亡的患者的冠状动脉病变中也发现了大量中性粒细胞。中性粒细胞浸润达到峰值的时间早于CD68+巨噬细胞、CD3+T淋巴细胞和CD20+B淋巴细胞的峰值。结论：这些结果提示中性粒细胞参与了KD早期冠状动脉的损伤。血管舒张可能是由于中性粒细胞和巨噬细胞引起的血管壁损伤而发生的。
Background: There has been no morphological evidence that polymorphonuclear leukocytes (PMNL) infiltrate the coronary arterial lesions of acute Kawasaki disease (KD) patients, although clinical data indicate the activation of PMNL.Methods: The experimental materials consisted of eight autopsy patients who died during the acute phase of KD. Duration of the illness ranged from 6 to 32 days. 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 and neutrophil elastase were used for immunohistochemistry to identify infiltrating cells in arterial lesions.Results: The inflammatory cells that 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+ T lymphocytes and CD20+ B lymphocytes.Conclusions: These results suggest that neutrophils are involved in the damage occurring to coronary arteries in the early stage of KD. Vasodilation might occur as a result of injury to vascular walls caused by neutrophils, as well as macrophages.