Neutrophil activation and subsequent endothelial cell injury play a key role in the pathogenesis of coronary artery lesions in Kawasaki disease.
Neutrophil-targeted therapies merit exploration in Kawasaki disease; leaves open whether this reduces lesions in prospective trials.
In the acute phase of Kawasaki disease (KD), there is an increase in the number of circulating neutrophils, including toxic neutrophils, which are caused by a morphological change. The functions of the neutrophils are also activated, leading to the excessive production of reactive oxygen species and elastase, which may induce endothelial cell (EC) injury. Histological findings demonstrate that numerous neutrophils infiltrate into coronary artery lesions (CALs) during the early phase of KD. Thus, it is suggested that neutrophil-mediated EC injury may be involved in the formation of CALs in KD patients. In this review, we focus on the role of neutrophil activation in the pathogenesis of KD vasculitis and discuss the methods of treatment for neutrophil-mediated EC injury.
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Takeshita et al. (2018) studied this question.
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