Regulation of the expression of Fcγ receptor on circulating neutrophils and monocytes in Kawasaki disease

Abstract

To investigate the regulation of Fc gamma receptor (Fc gamma R) expression on circulating phagocytes in Kawasaki disease (KD), we analysed the expressions of Fc gamma RI, II and III on neutrophils and monocytes in 20 patients with KD, 10 with a bacterial infection (BI), 10 with a viral infection (VI), and 10 healthy controls (HC) using flow cytometric analysis. The KD patients had a significantly higher level of Fc gamma RI expression on neutrophils, but not on monocytes, than the BI, VI and HC patients. Fc gamma RII expression on neutrophils was significantly higher in KD, BI and VI than HC, but there was no significant difference in Fc gamma RII expression among KD, BI and VI. Fc gamma RIII expression on neutrophils in KD was significantly lower than in VI and HC, but was higher on monocytes. A kinetic analysis of Fc gamma R expression in KD demonstrated the expression of Fc gamma RI and II on neutrophils to decline, but no remarkable change was observed in the monocytes, from the subacute phase through the convalescent phase. In addition, Fc gamma RIII expression on neutrophils increased, while Fc gamma RIII expression on monocytes decreased during the time course of KD. Fc gamma R expression in the acute phase of KD is thus characterized by markedly increased expression of Fc gamma RI on neutrophils, followed by a subsequent decrease, and decreased expression of Fc gamma RIII on neutrophils and increased expression of Fc gamma RIII on monocytes followed by a reverse kinetics during the clinical course. These findings are thus considered to reflect the functional up-regulation of neutrophils and monocytes in KD.

Neutrophilic involvement in the damage to coronary arteries in acute stage of Kawasaki disease

“…The mechanism by which high‐dose immunoglobulin ameliorates the vasculitis of KD remains obscure. The possibilities include blockade of immunological activation of the inflammatory response directed to vascular surfaces, saturation of Fc receptors on endothelial cells or phagocytes, or provision of a specific antibody to counteract an unidentified causal agent of KD 15,16 . In contrast, Zaitsu et al .…”

The Role of Neutrophil Activation in the Pathogenesis of Kawasaki Disease

“…The CD11b expression of circulating neutrophils was increased in the acute phase of KD and was positively correlated with the serum levels of IL-6, IL-10, and granulocyte colony-stimulating factor (G-CSF) [22]. The expression of CD64 (FcγR) of neutrophils is reported to dramatically increase in the acute phase of KD and to decrease after IVIG infusion [23,24]. Since neutrophils primed in vitro with IFN-γ and G-CSF can induce the expression of CD64 [25,26], the up-regulation of CD64 may reflect the activation of neutrophils by inflammatory cytokines.…”

Macrophage development and polarization in chronic inflammation

“…Kawasaki disease is an acute inflammatory disease of the arteries, which affects children and can lead to formation of aneurysms of the coronary arteries. In the acute phase of the disease, an expansion of the CD14 low /CD16 ++ monocytes has been described [144][145][146]. Interestingly, treatment of the disease involves infusion of high doses of Ig, the mechanism of action of which has been linked to blockade of FcRs [147].…”