Kawasaki disease (KD) is an acute
systemic vasculitis of an unknown aetiology. A small proportion of children exposed to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) or infected by Yersinia reproducibly develop principal symptoms of KD in various ethnic areas, but not in all studies. These microbes provoke a rapid cell-damaging process, called 'pyroptosis', which is characterised by a subsequent release of proinflammatory cellular components from damaged endothelial and innate immune cells. In agreement with these molecular events, patients with KD show elevated levels of damage-associated molecular patterns derived from cell death. In addition, an overwhelming amount of oxidative stress-associated molecules, including oxidised
phospholipids or
low-density lipoproteins, are generated as by-products of
inflammation during the acute phase of the disease. These molecules induce abnormalities in the acquired immune system and activate innate immune and vascular cells to produce a range of proinflammatory molecules such as
cytokines,
chemokines,
proteases and
reactive oxygen species. These responses further recruit immune cells to the arterial wall, wherein
inflammation and oxidative stress closely interact and mutually amplify each other. The
inflammasome, a key component of the innate immune system, plays an essential role in the development of
vasculitis in KD. Thus, innate immune memory, or 'trained immunity', may promote
vasculitis in KD. Hence, this review will be helpful in understanding the pathophysiologic pathways leading to the development of principal KD symptoms and coronary artery lesions in patients with KD, as well as in subsets of patients with SARS-CoV-2 and
Yersinia infections.