A novel anti-peroxiredoxin autoantibody in patients with Kawasaki disease
Article first published online: 13 FEB 2012
© 2012 The Societies and Blackwell Publishing Asia Pty Ltd
Microbiology and Immunology
Volume 56, Issue 1, pages 56–61, January 2012
How to Cite
Fujieda, M., Karasawa, R., Takasugi, H., Yamamoto, M., Kataoka, K., Yudoh, K., Kato, T., Ozaki, S. and Wakiguchi, H. (2012), A novel anti-peroxiredoxin autoantibody in patients with Kawasaki disease. Microbiology and Immunology, 56: 56–61. doi: 10.1111/j.1348-0421.2011.00393.x
- Issue published online: 13 FEB 2012
- Article first published online: 13 FEB 2012
- Accepted manuscript online: 17 OCT 2011 05:38AM EST
- Received 21 July 2011; revised 28 September 2011; accepted 30 September 2011.
- Kawasaki disease;
- oxidative stress;
- 8-isoprostaglandin F2α
Antibodies to the anti-oxidative peroxiredoxin (Prx) enzymes occur in both systemic autoimmune disease and vasculitis in adulthood. Because increased oxidative stress induces vasculitis in Kawasaki disease (KD), autoimmunity to Prxs in patients with KD was investigated. The presence of antibodies to Prx 1, 2 and 4 was analyzed by ELISA and Western blot. Of 30 patients with KD, 13 (43.3%) possessed antibodies to Prx 2, whereas these antibodies were present in only 1 of 10 patients (10.0%) with sepsis (4 with purulent meningitis and 6 with septicemia). In contrast, antibodies to Prx 1 and 4 were not detected in either group. There was no significant correlation among the titers of the three antibodies. Clinical parameters were compared between anti-Prx 2-positive and -negative patients. The presence of anti-Prx 2 antibodies correlated with a longer period of fever and poor response to high-dose γ-globulin therapy in patients with KD. Anti-Prx 2-positive patients had significantly greater excretion of urinary 8-isoprostaglandin than did anti-Prx 2-negative patients. These results provide the first evidence for an antibody to Prx 2 in patients with KD. They also suggest that this antibody might serve as a marker of disease severity and be involved in the pathophysiology of vasculitis in some patients with KD.