Dr Helen Williams^1,2, Dr Sasithorn Suda², Mr Suat Dervish³, Yen Tien Yap², Dr Heather Medbury^1,2, Professor Andrew Holland⁴

¹Westmead Hospital, Westmead, Australia, ²Westmead Clinical School, The University of Sydney, Westmead, Australia, ³Westmead Research Hub, Westmead Institute for Medical Research, Westmead, Australia, ⁴The Children’s Hospital Burns Research Institute, The Children’s Hospital at Westmead Clinical School, The University of Sydney, Westmead, Australia

Abstract:

Introduction: Hypertrophic scars (HTS) remain a common outcome of paediatric burns. Some factors contributing to HTS are well established, but understanding other contributors could aid in HTS risk assessment and enable more targeted treatment. As wounds heal, there is a sequential elevation in M1 macrophages (inflammation), followed by M2 macrophages (remodelling): dysregulation of this results in poor healing. This may help to explain HTS, as scar tissue shows elevated levels of fibrocytes, M2-like cells.

Objectives: To determine whether alterations in M1/M2 profile of monocytes, or fibrocyte numbers, are associated with healing outcomes and development of HTS.

Methods: Paediatric patients (0-16 years) attending for burn treatment and controls presenting for elective surgery were recruited. A single blood sample was taken and whole blood flow cytometry used to determine monocyte M1 and M2 markers levels and circulating fibrocyte numbers. Participants were divided into No-HTS and HTS groups based on scar assessment at 12 months, and comparisons made between groups.

Results: Burns patients (n=9 HTS, n=8 No-HTS) and controls (n=16) were included. The HTS group had a significantly higher ratio of M1/M2 (CD86/CD200R) ratio (p<0.05), indicating a higher M1 relative to M2 profile associates with HTS. Additionally, the M1 marker (CD120b) showed a positive correlation with healing time, indicating an elevated M1 response post-burn could contribute to delayed healing. Fibrocytes did not differ between groups.

Conclusion: Increased inflammatory (M1) response is likely to contribute to delayed healing and HTS. Further studies may assess suitability of monocyte profile for prediction of HTS.

Biography:

Helen is a part-time Senior Scientific Officer at Westmead Hospital and holds a Research affiliation with The University of Sydney. Her main interest is monocyte alterations in a range of disease states. Originally focussing on cardiovascular diseases, she is developing a growing interest in wound healing.

She enjoys sharing her work with the broader community through science outreach activities, and uses her two young children as an excuse to watch kids TV shows.