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Updated: Jul 8, 2026

A Swine Burn Model for Investigating the Healing Process in Multiple Depth Burn Wounds
Published on: February 23, 2024
Delayed inflammatory resolution and TGF-beta expressing Tregs are associated with healing outcomes in paediatric
Donna Langley1, Andrew J A Holland2, Giorgio Stefanutti3
1School of Biomedical Sciences, Faculty of Health, Queensland University of Technology (QUT), Centre for Children's Health Research, South Brisbane, Queensland, Australia; Centre for Immunology and Infection Control (CIIC), QIMR Berghofer Medical Research Institute, Queensland University of Technology (QUT), Brisbane, Queensland, Australia; Centre for Biomedical Technology (CBT), Queensland University of Technology (QUT), Kelvin Grove, Queensland, Australia.
Insights
Delayed wound healing in pediatric burn patients is linked to specific immune cell changes. Elevated pro-inflammatory cytokines like IL-17 and IL-23 in T cells and increased CCR6 expression indicate a persistent inflammatory state.
Area of Science:
- Immunology
- Pediatric Burn Research
- Wound Healing
Background:
- Delayed wound healing is a significant complication in pediatric burn patients.
- Understanding the underlying immune mechanisms is crucial for developing effective treatments.
Purpose of the Study:
- To identify immune cells and inflammatory mediators associated with delayed wound healing in pediatric burn patients.
- To compare immune profiles between healthy controls, normally healing burn patients, and delayed healing burn patients.
Main Methods:
- Isolation of peripheral blood mononuclear cells (PBMCs) from 30 pediatric participants.
- Flow cytometry to quantify immune cell subsets and intracellular cytokine expression.
- Multiplex immunoassay to measure plasma cytokine concentrations.
Main Results:
- No significant differences in major immune cell subsets were observed between groups.
- Delayed healing patients showed higher CCR6⁺ cell frequencies and elevated IL-17/IL-23 expression in specific T cell subsets.
- Increased plasma levels of IL-33, IL-23, TNF-α, and MCP-1 were found in the delayed healing group.
- Normal healing patients had higher proportions of regulatory T cells (Tregs) expressing TGF-β.
Conclusions:
- Delayed healing in pediatric burn patients is associated with a persistent systemic pro-inflammatory immune profile.
- Elevated CCR6 expression and IL-17/IL-23 axis activation may contribute to chronic immune dysregulation.
- Targeting these inflammatory pathways could offer novel therapeutic strategies for improving pediatric burn wound healing.
Abstract:
The aim of this study was to identify immune cells and inflammatory mediators associated with delayed wound healing in paediatric burn patients. Peripheral blood mononuclear cells (PBMCs) were isolated from 30 paediatric participants: 10 healthy age- and sex-matched controls, 10 burn patients whose wounds healed within 21 days (normal healing), and 10 patients with healing times exceeding 21 days (delayed healing). Flow cytometry was used to quantify immune cell subsets and intracellular cytokine expression, and plasma cytokines were measured via multiplex immunoassay. There were no significant differences in the proportions of major immune cell subsets-including CD4⁺ T-helper cells, CD8⁺ cytotoxic T cells, monocytes, and macrophages-between the groups. However, delayed healing patients exhibited significantly higher frequencies of CCR6⁺ cells and elevated expression of pro-inflammatory cytokines IL-17 and IL-23 in γδ T cells, NKT-like cells, and regulatory T cells (Tregs). Plasma concentrations of IL-33, IL-23, TNF-α, and MCP-1 were also significantly increased in the delayed healing group (p < 0.05). In contrast, patients with normal healing displayed higher proportions of Tregs expressing the anti-inflammatory cytokine TGF-β. These findings suggest that delayed healing in paediatric burn patients may be associated with a persistent systemic pro-inflammatory immune profile, marked by elevated CCR6 expression and IL-17/IL-23 axis activation. This unresolved inflammation could contribute to chronic immune dysregulation and may underlie the long-term comorbidities observed in this population. Targeting these inflammatory pathways may offer novel therapeutic strategies to improve wound healing outcomes in paediatric burns.
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