Sera from patients with Kawasaki disease induce intercellular adhesion molecule-1 but not Fas in human endothelial cells.

Background: Kawasaki disease (KD) is an acute vasculitis of unknown etiology occurring in childhood, characterized by abnormalities of the immune system including elevations of proinflammatory cytokines in the serum. We investigated the effect of serum from patients with KD on the expression of intercellular adhesion molecule-1 (ICAM-1) and Fas by human umbilical vein endothelial cells (HUVEC).
Methods: Confluent monolayers of HUVEC were incubated with sera from patients in the acute or convalescent phase of KD. Expression of ICAM-1 and Fas by HUVEC was assessed by flow cytometry. Concentrations of tumor necrosis factor (TNF)-alpha and interleukin (IL)-1beta in sera from patients with KD were measured by an immunoradiometric assay and an enzyme-linked immunosorbent assay, respectively.
Results: Sera from patients in the acute phase of KD produced significantly greater ICAM-1 expression by HUVEC than sera from patients in the convalescent phase. In contrast, KD sera did not induce Fas expression. While the mean serum concentration of TNF-alpha in patients in the acute phase of KD was significantly higher than in those in the convalescent phase, IL-1beta concentrations did not differ between the acute and convalescent phases. Exposure of HUVEC to recombinant human TNF-alpha increased the expression of both ICAM-1 and Fas, but a much lower concentration was required for an effect upon ICAM-1. Exogenous TNF-alpha did not induce apoptosis in HUVEC.
Conclusions: These results suggest that increased expression of ICAM-1 by endothelial cells might be involved in the pathogenesis of acute KD, and that TNF-alpha might induce ICAM-1 expression.
(Copyright 2001 S. Karger AG, Basel.)