Oxidative Stress in Kawasaki Disease

Abstract

Because inflammation and oxidative stress are closely related, oxidative stress cannot be ignored when considering pathologic conditions associated with inflammation-based Kawasaki disease (KD). KD pathogenesis is triggered by certain unknown infectious factors that activate one or multiple inflammation pathways via intricately intertwined cytokine cascades. Overproduction of reactive oxygen species from activated inflammation pathways increases oxidative stress in the body and results in an endless vicious cycle between inflammation reactions and reactive oxygen, which presumably underlies the diffuse vasculitis formed during acute KD. Although vascular inflammation and oxidative stress can be rapidly suppressed by treatment during the acute phase, they may persist in various forms for a long time. This has recently been identified as a concern in late KD. Generally, the presence of vascular inflammation and oxidative stress impairs blood vessels, leading to atherosclerosis onset, a widely recognized risk (Li et al., Atherosclerosis 237(1):208–219, 2014). This chapter will focus on determining whether the same is valid for blood vessels in late KD.