Recent experimental data and clinical, genetic, and transcriptome evidence from patients converge to suggest a key role of interleukin-1β (IL-1β) in the pathogenesis of Kawasaki disease (KD).
These data provide new mechanistic insights into the contributions of S100A12 and IL-1β to disease pathogenesis, and may therefore support current IL-1-targeting studies in the treatment of patients with KD.
Thus, TNF and IL-1 appear to play temporally distinct roles in KD, with TNF being active in acute cardiac inflammation and IL-1 in the subsequent development of coronary vasculitis.
This study is among the first to report epigenetic hypomethylation, increased transcripts, and the upregulation of NLRC4, NLRP12 and IL-1β in KD patients.
Furthermore, serum CTRP1 levels were positively correlated with the time point of intravenous immunoglobulin (IVIG), WBC, N%, TNF-α, IL-1β, and IL-6 levels in the KD-CAL group.ConclusionCTRP1 may participate in the process of vasculitis and blood coagulation during the acute phase of KD.
In conclusion, QUC inhibits both the NLRP3 and AIM2 inflammasome by preventing ASC oligomerization and may be a potential therapeutic candidate for Kawasaki disease vasculitis and other IL-1 mediated inflammatory diseases.
Both IL-1α and IL-1β have been shown to induce myocarditis and aneurysm formation in <i>Lactobacillus casei</i> cell-wall extract mouse model of KD; both being successfully improved with IL-1 blockade treatment such as anakinra.
This study investigated the relationship between serum levels of IL-27, Interleukin-17A (IL-17A), Interleukin-10 (IL-10), Interleukin-6 (IL-6), Interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α) and coronary artery lesions (CALs) in patients with KD.
Serum TNF-alpha levels are elevated in KD, which might activate the endothelial cells to express intercellular adhesion molecule-1 (ICAM-1), vascular cellular adhesion molecule-1(VCAM-1), inducible nitric oxide synthase (iNOS) and IL-1β.
Our findings provide the mechanism behind the observed efficacy of rescue therapy with IL-1 blockade in recalcitrant KD, and we identify that regulation of calcium mobilization is fundamental to the underlying immunobiology in KD.
This study aimed to examine whether coding single-nucleotide polymorphisms (cSNPs) of the interleukin-1 gene cluster [interleukin-1-alpha (IL1α), IL1β, IL-1-receptor antagonist (IL1RN)] are genetic markers of susceptibility to Kawasaki disease (KD) in the Korean population.
The results also underscore the importance of the IL-1 pathway as a mediator of inflammation in KD and suggest that IL-1 or its receptor may be reasonable targets for therapy, particularly for IVIG resistant patients.
The purpose of this study was to evaluate whether IL-1 beta (IL-1beta promoter and IL-1beta exon 5), IL-1 receptor antagonist (IL-1 Ra), and IL-4 (IL-4 promoter and IL-4 intron 3) gene polymorphisms act as markers of susceptibility to Kawasaki disease (KD), or of the severity of the disease.