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.
Several studies have established that blocking TNF-α is critical for obtaining anti-inflammatory effects in children with KD, thus, there is a need to identify benefits and risks of TNF-α blockers for the treatment of KD.
Furthermore, in the mouse model of KD, AUDA reduced the protein expression of MMP-9, IL-1β and TNF-α, indicating that AUDA may alleviate inflammatory reactions in the coronary arteries of KD model mice.
Infliximab, a monoclonal antibody directed against tumor necrosis factor-α, is being evaluated as adjunctive therapy to intravenous immunoglobulin (IVIG) for treatment of young children with acute Kawasaki disease (KD).
We measured the in vitro production of interferon (IFN)-γ, tumour necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, IL-1 receptor antagonist (IL-1ra), and IL-10 following whole blood stimulation with toll-like receptor and inflammasome ligands in 52 KD, 20 TSS, and 53 control participants in a case-control study.
Serum CTRP1 levels in all subjects and serum tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6) levels in KD patients were measured using enzyme-linked immunosorbent assay.ResultsCompared with the HC group, serum CTRP1 levels were significantly elevated in the KD group.
Clinical significance of serum soluble TNF receptor II level and soluble TNF receptor II/I ratio as indicators of coronary artery lesion development in Kawasaki disease.
PTX3 and TNF-α were rarely detected and only in trace concentration in KD, and the levels of IL-6 were not different from those of nonspecific viral illnesses.
The expression of TNFα, interleukin-6 and C-reactive protein were all increased in the livers of tumor-bearing mice, and KD significantly boosted their expression.
TNF-α as well as conventional inflammatory mediators could not be used to differentiate the clinical classification of KD, but they may prove beneficial to heighten or reduce the suspicion of incomplete KD.
SN50, an NF-κB inhibitor, significantly attenuated caspase-4 expression, secretion of IL-6, IL-1β, and TNF-α, as well as HCAEC apoptosis in cells treated with KD patient PBMC-conditioned media.
In this study, firstly we verified the overexpressed TNF-α in KD patients, and found TNF-α was able to induce HUVECs apoptosis and inhibit HUVECs proliferation.
Our data showed significant deviations between patients with Kawasaki disease and controls concerning the TNF -308 polymorphism genotype (GG: P = 0.0449) and allele (G,A: P = 0.0433) and -238 polymorphism genotype frequencies (AA: P = 0.0351).
Infliximab (IFX), a known monoclonal antibody against tumor necrosis factor-α (TNF-α), is used to treat Kawasaki disease (KD) patients with intravenous immunoglobulin (IVIG) resistance.
We found higher expression levels of proinflammatory cytokines from MC, such as IL-1β, IL-6 and TNF-α in patients with KD compared with the healthy controls (P < 0.05).
This study determined the association of TNF -308 and lymphotoxin-alpha (LTA) +252 polymorphisms in Mexican pediatric patients with KD and coronary aneurysms (CA).
Tumor necrosis factor (TNF) and the TNF receptor superfamily (TNF-TNFR) plays very important roles in the pathogenesis of Kawasaki disease (KD) by leukocyte recruitment, upregulation of matrix-degrading enzymes and proinflammatory cytokines.
Our findings suggest that CRP +1444 C-->T and TNF-alpha -308 G-->A polymorphisms are associated with predisposition to Kawasaki disease and, in patients with Kawasaki disease, increased carotid arterial stiffness and intima-media thickness in the long-term.