Abstract

To assess the association of nuclear factor-kappa B (NF-κB) and complications of Kawasaki disease (KD) in Chinese children. Based on color Doppler examination results, 86 affected children in the KD group were divided into two groups: 39 cases in coronary artery lesion group (CALs subgroup) and 47 cases in non-coronary artery lesion group (Non-CALs subgroup). Infection control group consisted of 65 cases of hospitalized infected children with fever, having same age as the affected children. Healthy control group consisted of 102 cases of healthy children of the same age, visiting the hospital for physical examination. Western blot was used to detect the expression of NF-кBp65 and IкBα proteins in periphery blood mononuclear cells (PBMC); reverse transcription polymerase chain reaction (RT-PCR) was used to detect the expression of TNF-α and MCP-1 mRNA. The value of NF-kBp65 (optical density) in the PBMC cell nuclei in the KD group was significantly higher than that in the two control groups (p < 0.01). The value of NF-κBp65 in the CALs subgroup was significantly higher than that in the Non-CALs subgroup (p < 0.05). The value of NF-κBp65 inhibitor IκBα in the KD group was significantly lower than that in the infection control group and the healthy control group (p < 0.01). There was a positive correlation between the ratio nucleus NF-κBP65/ IκBα and the severity degree of CALs(r = 0.536, p < 0.05). The value of TNF-α mRNA (O.D ratio) in the KD group was significantly higher than that in the two control groups (P < 0.01), and the value of TNF-α mRNA in the CALs subgroup was significantly higher than that in the Non-CALs subgroup (P < 0.05). The value of MCP-1 mRNA in the KD group was significantly higher than that in the two control groups (P < 0.01), and the value of MCP-1 mRNA in the CALs subgroup was significantly higher than that in the Non-CALs subgroup (P < 0.05). NF-κBp65 participates in the pathogenesis of vasculitis of KD in acute stage, and may aggravate the vasculitis in KD and plays a part in the formation of CALs.

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