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Published on: March 24, 2017
Inhibition of IRF8 Negatively Regulates Macrophage Function and Impairs Cutaneous Wound Healing
Yuanyuan Guo1, Zhiyin Yang2, Shan Wu1
1Department of Burns and Plastic Surgery, Shanghai Ninth People's Hospital, Institute of Traumatic Medicine, Shanghai Jiao Tong University School of Medicine, 280 Mohe Road, Baoshan District, Shanghai, 201900, China.
Abstract:
The inflammatory response is essential for normal cutaneous wound healing. Macrophages, as critical inflammatory cells, coordinate inflammation and angiogenesis phases during wound healing. It has been reported that the transcription factor interferon regulatory factor 8 (IRF8), a member of the IRF family, plays a critical role in the development and function of macrophages and is associated with inflammation. However, the role of IRF8 in cutaneous wound healing and its underlying mechanism remain elusive. Through immunohistochemical (IHC) staining, we showed that IRF8 is involved in the wound repair process in mice and patients. Furthermore, we ascertain that the repression of IRF8 by small interfering RNA (siRNA) leads to delayed wound healing. To explore the mechanism by which IRF8 impacts wound healing, we observed its effect on macrophage-related mediators by IHC or real-time PCR. The results demonstrated that the inhibition of IRF8 decreases the mRNA expression of inflammatory mediators associated with M1 macrophage (il-1b, il-6, inos, and tnf-a) but no impact on M2 macrophage-related mediators (arg-1, mrc-1, and il-10) and the number of macrophages in the wounds. Furthermore, the inhibition of IRF8 induced apoptosis in the wounds. In summary, this study demonstrates that the down-regulation of IRF8 in the wound leads to impaired wound healing possibly through the regulation of macrophage function and apoptosis in skin wound.
Insights
Interferon regulatory factor 8 (IRF8) is crucial for skin wound healing. Its repression delays healing by affecting M1 macrophage function and increasing apoptosis, highlighting IRF8
Area of Science:
- Dermatology
- Immunology
- Molecular Biology
Background:
- Cutaneous wound healing relies on inflammatory responses coordinated by macrophages.
- Interferon regulatory factor 8 (IRF8) influences macrophage development and inflammation.
- The specific role of IRF8 in skin wound repair remains unclear.
Purpose of the Study:
- To investigate the role of IRF8 in cutaneous wound healing.
- To elucidate the underlying mechanisms of IRF8's involvement in skin repair.
Main Methods:
- Immunohistochemical (IHC) staining to detect IRF8 in wound tissues.
- Small interfering RNA (siRNA) to inhibit IRF8 expression.
- Real-time PCR and IHC to analyze macrophage-related mediators.
Main Results:
- IRF8 expression was detected during the wound repair process in mice and human patients.
- IRF8 inhibition via siRNA resulted in delayed wound healing.
- IRF8 suppression reduced M1 macrophage-associated inflammatory mediators (IL-1β, IL-6, iNOS, TNF-α) but did not affect M2 markers.
- IRF8 inhibition led to increased apoptosis in wound tissues.
Conclusions:
- IRF8 plays a significant role in promoting cutaneous wound healing.
- Down-regulation of IRF8 impairs skin wound repair, potentially by modulating M1 macrophage activity and inducing apoptosis.
