2003 Fiscal Year Final Research Report Summary
Histopathological study on developmental mechanism of the coronary, artery destruction in acute stage Kawasaki Disease patients
Project/Area Number |
14570168
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Human pathology
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Research Institution | Toho University |
Principal Investigator |
TAKAHASHI Kei Toho University, School of Medicine, Associate Professor, 医学部, 助教授 (80216712)
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Project Period (FY) |
2002 – 2003
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Keywords | Kawasaki disease / Coronary arteritis / Coronary artery aneurysm / Immunoglobulin / Neutrophils / Immunohistochemistry / Systemic vasculitis / Plasma cells |
Research Abstract |
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.
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Research Products
(12 results)