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

Research Project

Project/Area Number 14570168
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Human pathology
Research InstitutionToho University

Principal Investigator

TAKAHASHI Kei  Toho University, School of Medicine, Associate Professor, 医学部, 助教授 (80216712)

Project Period (FY) 2002 – 2003
Project Status Completed (Fiscal Year 2003)
Budget Amount *help
¥2,400,000 (Direct Cost: ¥2,400,000)
Fiscal Year 2003: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 2002: ¥1,100,000 (Direct Cost: ¥1,100,000)
KeywordsKawasaki 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
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.

Report

(3 results)
  • 2003 Annual Research Report   Final Research Report Summary
  • 2002 Annual Research Report
  • Research Products

    (21 results)

All Other

All Publications (21 results)

  • [Publications] 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)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2003 Final Research Report Summary
  • [Publications] 高橋 啓: "小児血管炎の病理"病理と臨床. 21. 926-927 (2003)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2003 Final Research Report Summary
  • [Publications] 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)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2003 Final Research Report Summary
  • [Publications] 高橋 啓, 大原関 利幸, 他: "カンジダ菌体抽出物によるマウス系統的血管炎誘発モデルと川崎病"脈管学. 43. 673-678 (2003)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2003 Final Research Report Summary
  • [Publications] K.Takahashi, et al.: "Histopathological features of murine systemic vasculitis caused bv Candida albicans extract - an animal model of Kawasaki Disease."Inflammation Research. 53. 72-77 (2004)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2003 Final Research Report Summary
  • [Publications] 高橋 啓, 直江 史郎: "分子誘導型モデル動物-Candida albicans菌体成分による動脈炎誘発モデル"医学のあゆみ. 206. 147-149 (2003)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2003 Final Research Report Summary
  • [Publications] 高橋 啓, 直江史郎(分担): "動脈癌と動脈解離の最前線"医歯薬出版、東京. 186 (2001)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2003 Final Research Report Summary
  • [Publications] Takahashi Kei, et al.: "Pathological study of post-coronary arteritis in adolescents and young adults: with reference to the relationship between sequelae of Kawasaki disease and atherosclerosis."Pediatr Cardiol. 22. 138-142 (2001)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2003 Final Research Report Summary
  • [Publications] Takahashi Kei: "The possibility of progressing to the stenotic lesions at non-anuerysmal coronary arteries in Kawasaki disease."Prog.Med.. 22. 1676-1678 (2002)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2003 Final Research Report Summary
  • [Publications] Takahashi Kei: "Arterial lesions in Kawasaki disease."Byori-to-Rinsho. 21. 926-927 (2003)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2003 Final Research Report Summary
  • [Publications] Takahashi Kei, et al.: "A murine vasculitis caused by Candida albicans extract and vasculitis in Kawasaki disease."J.Jpn.Coll.Angiol.. 46. 673-678 (2003)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2003 Final Research Report Summary
  • [Publications] 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)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2003 Final Research Report Summary
  • [Publications] 高橋 啓: "小児血管炎の病理"病理と臨床. 21. 926-927 (2003)

    • Related Report
      2003 Annual Research Report
  • [Publications] 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)

    • Related Report
      2003 Annual Research Report
  • [Publications] 高橋 啓, 大原関利章, 他: "川崎病の心血管にはどのような病理組織学的変化がみられるか"小児内科. 35. 1497-1499 (2003)

    • Related Report
      2003 Annual Research Report
  • [Publications] 高橋 啓, 大原関利章, 他: "カンジダ菌体抽出物によるマウス系統的血管炎誘発モデルと川崎病"脈管学. 43. 673-678 (2003)

    • Related Report
      2003 Annual Research Report
  • [Publications] 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)

    • Related Report
      2003 Annual Research Report
  • [Publications] 高橋 啓, 直江史郎: "分子誘導型モデル動物-Candida albicans菌体成分による動脈炎誘発モデル"医学のあゆみ. 206. 147-149 (2003)

    • Related Report
      2003 Annual Research Report
  • [Publications] 高橋 啓: "瘤を確認できなかっ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)

    • Related Report
      2002 Annual Research Report
  • [Publications] 高橋 啓, 大原関利章, 直江史郎: "動脈と大動脈の解剖と病理"Medicina. 39. 1450-1452 (2002)

    • Related Report
      2002 Annual Research Report
  • [Publications] 高橋 啓, 直江史郎(分担): "川崎病冠状動脈炎の病理組織像と動脈解離・未解離 動脈瘤と動脈解離の最前線"医歯薬出版、東京. 186 (2001)

    • Related Report
      2002 Annual Research Report

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Published: 2002-04-01   Modified: 2016-04-21  

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