Persistent immune dysregulation consistent with chronic low-grade inflammation in paediatric burn survivors.
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OBJECTIVES: To characterise long-term immune dysregulation and persistent inflammatory signalling in paediatric burn survivors with hypertrophic scarring. METHODS: Peripheral blood mononuclear cells and plasma were analysed from 20 paediatric participants: 10 burn survivors with hypertrophic scarring (median 4.1 years post-injury) and 10 age- and sex-matched healthy controls. Multiparameter flow cytometry, multiplex cytokine analysis, and quantitative reverse-transcription polymerase chain reaction (qRT-PCR) were used to assess immune cell phenotypes, inflammatory mediators, and inflammatory gene expression. RESULTS: Overall proportions of major immune cell subsets were comparable between groups. However, burn survivors with hypertrophic scarring demonstrated increased CD4⁺TNFα⁺ cells, Th17 cells, CCR6⁺ natural killer T-like cells, IL-23⁺ natural killer cells, and IL-23-expressing macrophage populations (all P < 0.05). Regulatory T cells (Tregs) and CCR4⁺CCR6⁺ double-positive Tregs were also increased (P < 0.05). Plasma concentrations of IL-1β, tumour necrosis factor-α, IL-12p70, IL-17A, and IL-23 were significantly elevated in the scar group (all P < 0.05). Gene expression analysis identified persistent upregulation of nuclear factor kappa B1 (NFκB1; 2.21-fold) and IL-17 (3.38-fold). CONCLUSION: Paediatric burn survivors with hypertrophic scarring demonstrate persistent systemic immune dysregulation several years after injury. However, the cross-sectional design and absence of a normotrophic burn control group limit conclusions regarding whether these immune alterations are specific to pathological scarring or reflect broader long-term post-burn immune dysregulation.