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Updated: Oct 28, 2025
In Vitro Model of Human Cutaneous Hypertrophic Scarring using Macromolecular Crowding
Published on: May 1, 2020
Monocyte M1/M2 profile is altered in paediatric burn patients with hypertrophic scarring
Helen Williams1,2, Sasithorn Suda2, Suat Dervish3
1Department of Surgery, Westmead Hospital, Vascular Biology Research Centre, Westmead, Australia.
Insights
Increased monocyte inflammation, characterized by higher M1/M2 ratios, is linked to hypertrophic scar development in pediatric burn patients. This suggests monocyte profiles may predict poor wound healing outcomes and scarring.
Area of Science:
- Immunology
- Wound Healing
- Dermatology
Background:
- Hypertrophic scars (HTS) are a common complication of pediatric burn injuries.
- The development of HTS is associated with dysregulated wound healing, involving macrophages and fibrocytes.
- Monocytes, as progenitors of macrophages, can exhibit pro-inflammatory (M1) or anti-inflammatory (M2) phenotypes, influencing healing outcomes.
Purpose of the Study:
- To investigate whether monocyte profiles and fibrocyte counts can predict poor wound healing and hypertrophic scar formation in pediatric burn patients.
- To assess the correlation between monocyte subset proportions, M1/M2 marker expression, and healing time.
Main Methods:
- Blood samples were collected from pediatric burn patients and controls.
- Whole blood flow cytometry was used to quantify fibrocytes and monocyte subsets.
- M1 (CD86, CD120b, CD319) and M2 (CD93, CD163, CD200R) marker expression on monocytes was determined.
Main Results:
- Burn patients showed higher proportions of classical monocytes compared to controls.
- In patients with healing times >21 days, the hypertrophic scar group exhibited lower M2 (CD200R) expression and a significantly higher M1/M2 ratio (CD86/CD200R).
- M1 marker CD120b and the M1/M2 ratio (CD120b/CD200R) correlated positively with healing delay; fibrocyte counts did not differ significantly.
Conclusions:
- An elevated early inflammatory monocyte response, indicated by a higher M1/M2 ratio, is associated with the development of hypertrophic scars in pediatric burn patients.
- Monocyte inflammatory profiles, particularly M1 marker expression, may serve as indicators of delayed wound healing.
- Further research is needed to confirm the predictive value of monocyte profiles for hypertrophic scar development.
Abstract:
Hypertrophic scars (HTS) remain a common outcome of burn injury, particularly in children. They can arise from variations in the wound healing stages, such as an excessive inflammatory response or inefficient remodelling. Of the cells contributing to these healing stages, macrophages and fibrocytes are crucial. Specifically, the inflammatory phase is dominated by M1 macrophages, the proliferation/remodelling stages by M2 macrophages, and scar tissue contains numerous fibrocytes. As the progenitors to these cells, monocytes, can also exhibit M1- and M2-skewing, we proposed that their profile, or circulating fibrocyte counts, could be used to predict poor healing outcomes. To investigate this, we obtained blood samples from paediatric controls and burns patients, which were then divided into HTS and NoHTS groups upon scar assessment at 12 months. The samples were assessed by whole blood flow cytometry to quantify fibrocytes and monocyte subset proportions and to determine monocyte levels of M1 (CD86, CD120b, CD319) and M2 (CD93, CD163, CD200R) markers. Both burns groups had higher proportions of classical monocytes compared to controls, indicating increased cell turnover and/or entry of other subsets into the wound. In burns patients who took more than 21 days to heal, the HTS group had lower M2 (CD200R) expression with the ratio of M1/M2 (CD86/CD200R) being significantly higher. These results suggest an elevated early inflammatory monocyte response contributes to development of HTS. Correlations of marker expression with remaining healing time revealed a significant positive correlation with M1 (CD120b) and M1/M2 (CD120b/CD200R), suggesting a potential role for CD120b as an indicator of healing delay. Fibrocytes did not significantly differ between the groups. In conclusion, increased monocyte inflammation likely contributes to slower healing and development of scarring, but further studies are needed to determine the predictive power of monocyte inflammatory profile.
