Chronic wounds are a growing healthcare morbidity worldwide. Chronic wounds usually arise when one or more phases of wound-healing process is impaired or incomplete. Langerhans cells (LC) are a subset of dendritic cells whose primary function is antigen presentation and immune surveillance. In this study, we investigate the role of LC in the regulation of wound healing.
During normal wound healing, we observed that LC migrate out of the wound and repopulate the skin after a few days. LagDTR mice transgenic for the Diphtheria Toxin (DT) receptor under the control of a langerin/CD207+ promoter were used in this study, allowing for selective ablation of LC upon treatment with DT. Wounding was compared between mice with (LC+) or without (LC-) LCs that had been delivered a full-thickness skin wound (punch biopsy). Histological analysis and immunofluorescence (IF) staining was carried out to assess phenotypic changes between the two groups.
A comparison of the wounds between the LC+ and LC- groups revealed that wound healing was more rapid in the absence of LC. Martius scarlet blue (MSB) staining analysis revealed that re epithelialization was increased in LC- mice at days 3 and 6- post wounding. Proliferating cell nuclear antigen (PCNA) IF staining was carried out to confirm if the increased re epithelialization was mediated by keratinocyte proliferation but no significant difference was observed. There was a two-fold increase in angiogenesis in the absence of LC at day 6 confirmed by both MSB and IF staining.
From this we can conclude that LCs directly or indirectly mediate delayed wound healing, which may be contributed to by suppression of re epithelialization and angiogenesis. The results from this study can be extrapolated into future research for better understanding and management of individuals suffering from chronic wounds.