🩹 Why don't diabetic wounds heal?

Why do the wounds of people with diabetes have such difficulty closing? Seemingly simple wounds can become chronic, representing a significant medical problem. A recent scientific analysis indicates that a dysregulation in the behavior of immune cells could explain this difficulty.

This review, led by Yi Ru and colleagues, explores how various immune cells act during the healing phases. Published in MedScience, it demonstrates that the immune system, normally an ally in repair, malfunctions in diabetes.


Macrophages, essential for healing, illustrate this dysregulation well. Normally, they transition from an inflammatory state to a reparative state to resolve inflammation and rebuild tissues. In diabetic wounds, this transition often fails, leaving them stuck in an inflammatory phase. This prolongs damage and prevents healing, creating a vicious cycle where inflammation harms rather than helps.

Furthermore, other cells like neutrophils and mast cells contribute to this persistent inflammation. Neutrophils, the first to arrive at the injury site, release excess substances that worsen the damage. Mast cells, over-activated, maintain an unfavorable inflammatory environment. Together, these disturbances prevent the transition to the repair phase, leaving wounds open and vulnerable.

Dendritic cells and T lymphocytes also play an important role. In diabetic wounds, dendritic cells have difficulty clearing dead cells, leading to an accumulation of debris. Regulatory T lymphocytes, fewer in number and less effective, fail to control inflammation. These dysfunctions disrupt the coordination between innate and adaptive immune responses, hindering healing.

However, B cells can encourage macrophages to adopt a reparative state, while natural killer cells regulate inflammation and blood vessel formation. Their appropriate recruitment could offer opportunities for new therapeutic approaches by modulating the immune environment.

For the future, research continues to clarify the interactions between immune cells. A better understanding of these mechanisms could lead to more precise interventions, reducing the risk of amputation and improving the quality of life for people with diabetes. Hope rests on targeted therapies that restore the immune balance necessary for effective wound healing.

The normal functioning of macrophages in wound healing

Macrophages are central immune cells in tissue repair after an injury. Normally, they arrive at the wound site after neutrophils and first adopt a pro-inflammatory state, called M1, which helps fight infections and clear debris.

Then, they transition to a pro-reparative, or M2, state which promotes the resolution of inflammation and tissue reconstruction. This phase is essential for the formation of new blood vessels and the production of collagen, important elements for wound closure.

This change of state is regulated by chemical signals in the wound environment. When everything goes well, macrophages coordinate with other immune cells to ensure rapid and effective healing, without leaving excessive scarring.