ArticlePediatric research2026
Serum cytokine profiling reveals distinct inflammatory signatures in Kawasaki disease and MIS-C and suggests associations with coronary artery lesions.
Article in Pediatric research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
1 citing paper in PubMed.
- Metabolic reprogramming rewires aberrant immune responses to drive endothelial dysfunction in Kawasaki disease: a narrative review.Translational pediatrics · 2026Review
Corrections and comments
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Authors and funding
16 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundKawasaki disease (KD) is a systemic vasculitis that causes coronary artery lesions (CAL). Its clinical overlap with multisystem inflammatory syndrome in children (MIS-C) complicates differential diagnosis. The distinct immunopathologies and specific drivers of CAL, are not fully understood. This study aimed to clarify inflammatory cytokine differences between KD and MIS-C, and to identify molecules involved in CAL.
methodsWe measured 48 serum cytokines in 20 patients with KD (6 with CAL), 22 patients with MIS-C, and 9 healthy controls using a Luminex assay. The effects of cytokines on human coronary artery endothelial cells (HCAECs) were evaluated in vitro, assessing expression of angiogenic and adhesion molecules by RT-qPCR.
resultsFifteen cytokines differed significantly between KD and MIS-C. GRO-1α was the most effective biomarker for differentiation between KD and MIS-C. In KD, eight cytokines (including G-CSF, IL-6, and IL-17A) were elevated in cases with CAL. In vitro, IL-17A induced VEGF expression, IL-6 altered ANGPT1/2 balance, and G-CSF upregulated ICAM1 in HCAECs, suggesting distinct contributions to CAL development.
conclusionGRO-1α is a robust biomarker for distinguishing KD from MIS-C. IL-17A, IL-6, and G-CSF are key cytokines in CAL development. These findings advance KD pathogenesis understanding and may improve diagnosis and targeted therapies. IMPACT STATEMENT: GRO-1α (CXCL1) is identified as a novel biomarker that distinguishes Kawasaki disease (KD) from MIS-C. In patients with KD, elevated GRO-1α levels correlate with coronary artery lesion (CAL) development. In vitro, IL-6, IL-17A, and G-CSF induce pro-inflammatory responses in human coronary artery endothelial cells (HCAECs), linking these cytokines to vascular injury. GRO-1α and these cytokine pathways could serve as new biomarkers or therapeutic targets to increase diagnostic accuracy and prevent CAL. Targeting IL-6, IL-17A or G-CSF signaling may mitigate KD-associated vascular inflammation, suggesting new therapeutic strategies to reduce coronary damage.
Identifiers
42387075What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.