title: The role of TNF-α in a murine model of Kawasaki disease arteritis induced with a Candida albicans cell wall polysaccharide.
abstract: OBJECTIVE
  Various inflammatory cytokines, including tumor necrosis factor-α (TNF-α), have been reported to play roles in Kawasaki disease (KD). Recently, anti-TNF-α therapy was reported to show efficacy in patients who do not respond to high-dose intravenous immunoglobulin therapy. However, there are many gaps in our understanding of the role that TNF-α plays in the development of KD arteritis as well as whether anti-TNF-α therapy causes any histological changes in the arteritis. Accordingly, the present histopathological study was carried out to elucidate the inhibitory effect of anti-TNF-α therapy on vasculitis as well as the role of TNF-α in the development of vasculitis in a murine model of KD vasculitis.
  
  
  METHODS
  We used two anti-TNF-α drugs (etanercept and infliximab) to treat a Candida albicans-induced murine model of KD vasculitis. We investigated the histopathological changes in terms of the incidence of vasculitis, the scope of lesions and the degree of inflammation.
  
  
  RESULTS
  Administration of etanercept to the mice reduced not only the incidence of vasculitis but also the scope of lesions and the degree of inflammation.
  
  
  CONCLUSIONS
  Based on the histological findings, TNF-α is deeply involved in the development of vasculitis.
authors.affiliation: Department of Pathology, Toho University Ohashi Medical Center , 2-17-6 Ohashi, Meguro-ku, Tokyo 153-8515 , Japan.
authors.forename: Toshiaki
authors.initials: T
authors.lastname: Oharaseki
authors.forename: Yuki
authors.initials: Y
authors.lastname: Yokouchi
authors.forename: Hitomi
authors.initials: H
authors.lastname: Yamada
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Mamada
authors.forename: Satoshi
authors.initials: S
authors.lastname: Muto
authors.forename: Kiyomi
authors.initials: K
authors.lastname: Sadamoto
authors.forename: Noriko
authors.initials: N
authors.lastname: Miura
authors.forename: Naohito
authors.initials: N
authors.lastname: Ohno
authors.forename: Tsutomu
authors.initials: T
authors.lastname: Saji
authors.forename: Shiro
authors.initials: S
authors.lastname: Naoe
authors.forename: Kei
authors.initials: K
authors.lastname: Takahashi
mesh_terms: D000818:Animals; D000911:Antibodies, Monoclonal / Q000627:therapeutic use*; D001167:Arteritis / Q000139:chemically induced / Q000188:drug therapy* / Q000473:pathology; D002176:Candida albicans; D004195:Disease Models, Animal; D000068800:Etanercept; D007074:Immunoglobulin G / Q000627:therapeutic use*; D000069285:Infliximab; D051379:Mice; D009080:Mucocutaneous Lymph Node Syndrome / Q000139:chemically induced / Q000188:drug therapy* / Q000473:pathology; D009206:Myocardium / Q000473:pathology; D011134:Polysaccharides; D018124:Receptors, Tumor Necrosis Factor / Q000627:therapeutic use*; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors* / Q000378:metabolism
chemical_list: D000911:Antibodies, Monoclonal; D007074:Immunoglobulin G; D011134:Polysaccharides; D018124:Receptors, Tumor Necrosis Factor; D014409:Tumor Necrosis Factor-alpha; D000069285:Infliximab; D000068800:Etanercept