Exploring innate immunity in wound healing complications in RDEB patientsCompleted
|Project lead||Prof. Dr. Sabine Eming|
|Organisation||University Hospital of Cologne|
|Partner organizations & collaborators||Dr. Dimitra Kiritsi and Dr. Alexander Nystrom|
|Project budget||EUR 194,500|
|Start date / Duration||01. Jul 2018 / 36 months|
|Funder(s) / Co-Funder(s)||DEBRA UK, DEBRA Ireland, MSAP/EBEP Reviewed|
|Research area||Symptom prevention & relief|
Short lay summary
Cells of the immune system are an integral component of the body’s own or natural ability to restore tissue function after injury. After most types of tissue damage including blistering in EB patients, specific immune cells particularly monocytes and macrophages serve two key roles: to stop the damage and subsequently to help repair the tissue. Monocytes typically circulate in the blood for 1–3 days before migrating into tissues, where they become macrophages, there they eliminate harmful materials such as foreign substances, cellular debris and cancer cells.
The repair process requires macrophages to initially promote positive inflammation that aids cell defence, and then later when the immediate danger has passed to reduce inflammation to support resolution and repair. Previous research has shown that the tightly controlled dynamics between this pro-inflammatory and resolution response is fundamental for efficient healing.
This group plans to uncover the role of macrophages in wound healing in Recessive Dystrophic EB (RDEB) patients and to identify strategies to restore the function of these important cells in wounds of RDEB patients. Macrophages are also integrally linked to cancer formation and mechanistically they are likely placed at the interface between a poorly healing wound associated with RDEB and the potential for gradual transformation of the wound into cancer.
The aim of this project is to understand the fundamental mechanisms underpinning how immune cells assist and impair wound healing in RDEB patients to not only advance the development of new therapies that accelerate wound closure (e.g. wound dressings that may dampen chronic inflammation) but also to develop diagnostic tools to monitor when a poorly healing wound may become malignant or cancer forming.
This 3 year laboratory project will use samples from RDEB patients to establish the function of immune cells in the sequential stages of wound healing.
We believe that by increasing our understanding of how immune cells, in particular macrophages, function to facilitate the tissue repair response and to suppress scarring and carcinogenesis, that we will be able to improve the quality of life of individuals with RDEB.