title: Histopathological features of murine systemic vasculitis caused by Candida albicans extract--an animal model of Kawasaki disease.
abstract: OBJECTIVE
  We examined the histopathological features of systemic vasculitis caused in mice by injection of a Candida albicans ( C. albicans) extract and investigated the principal genetic roles in the development of vasculitis.
  
  
  METHODS
  C. albicans extract was injected intraperitoneally for five consecutive days in the 1st and 5th weeks to CD-1, C57BL/6N, C3H/HeN, BALB/cAnN, DBA/2N and CBA/JN mice. At week 8, mice were killed, and histological examination was performed by light microscopy.
  
  
  RESULTS
  Arteritis had developed in 66% of CD-1 mice. The extramural coronary arteries and aortic root close to the orifice of coronary arteries were most frequently involved. Histologically, the characteristic feature of the arteritis was proliferative and granulomatous inflammation accompanied by numerous macrophages, lymphocytes, plasma cells and neutrophils. Fibrocellular intimal thickening with destruction of the internal elastic lamina and media was also observed. Five mouse strains after injection of C. albicans extract were clearly classified into a resistant group (CBA/JN, DBA/2N and BALB/cAnN mice) and a sensitive group (C3H/HeN and C57BL/6N mice). The inbred mouse strains which showed the same histocompatibility-2 (H-2) haplotype exhibited a different susceptibility to development of vasculitis.
  
  
  CONCLUSIONS
  This arteritis murine model shows unique histological features that have not been observed in other animal vasculitis models and it most closely resembles Kawasaki disease in humans. The genetic control of susceptibility to induction of vasculitis by the C. albicans extract is dependent to the mouse strains, but is not linked to the H-2 loci.
authors.affiliation: Department of Pathology, Ohashi Hospital, Toho University School of Medicine, 2-17-6, Ohashi, Meguro, Tokyo, 153-8515, Japan. keitak@oha.toho-u.ac.jp
authors.forename: K
authors.initials: K
authors.lastname: Takahashi
authors.forename: T
authors.initials: T
authors.lastname: Oharaseki
authors.forename: M
authors.initials: M
authors.lastname: Wakayama
authors.forename: Y
authors.initials: Y
authors.lastname: Yokouchi
authors.forename: S
authors.initials: S
authors.lastname: Naoe
authors.forename: H
authors.initials: H
authors.lastname: Murata
mesh_terms: D000818:Animals; D001011:Aorta / Q000473:pathology; D001167:Arteritis / Q000382:microbiology / Q000473:pathology; D002176:Candida albicans; D003331:Coronary Vessels / Q000473:pathology; D004195:Disease Models, Animal; D020022:Genetic Predisposition to Disease; D008214:Lymphocytes / Q000473:pathology; D008264:Macrophages / Q000473:pathology; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D008809:Mice, Inbred C3H; D008810:Mice, Inbred C57BL; D008808:Mice, Inbred CBA; D008811:Mice, Inbred DBA; D008813:Mice, Inbred ICR; D009080:Mucocutaneous Lymph Node Syndrome / Q000473:pathology*; D009504:Neutrophils / Q000473:pathology; D010950:Plasma Cells / Q000473:pathology; D014657:Vasculitis / Q000235:genetics / Q000382:microbiology* / Q000473:pathology*