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IL-36Ra discovery may help heal skin wounds from ischemia reperfusion

The absence of interleukin-36 receptor antagonist (IL-36Ra) significantly slowed down wound healing in ischemia-reperfusion injuries in mice.

3D rendering of skin structure

A team from the Fujita Health University School of Medicine, Japan, have been investigating the role of interleukin-36 receptor antagonist (IL-36Ra) in in healing skin wounds from ischemia-reperfusion (I/R) injuries. They revealed that the absence IL-36Ra significantly slowed down wound healing in cutaneous I/R injuries, indicating a new therapeutic target.

“We wanted to understand the immunological mechanisms involved in the healing of wounds from cutaneous ischemia-reperfusion injuries, such as pressure ulcers and Raynaud’s phenomenon, to narrow down possible therapeutic targets,” explained Dr Yoshihito Tanaka who led the study. “Drawing from experience, IL-36Ra appeared to be a promising candidate for kickstarting our investigation.”

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The researchers used mice knocked out for the receptor and induced cutaneous I/R injuries in knockout and wild-type control mice. They then studied corresponding immunological responses in both groups of animals, including the time required for wound healing, infiltration of neutrophils/macrophages to the site of the wounds, apoptotic skin cells, and activation of other unwanted immunological defence mechanisms. 

diagram showing role of IL-36 in wound healing

Researchers studied the role of IL-36 receptor antagonist in wound healing caused by ischemia-reperfusion injury, using IL-36 knockout mice, compared to wildtype mice. [credit: Yoshihito Tanaka]

The results, published in the Journal of the European Academy of Dermatology and Venereology, showed that the absence of IL-36Ra significantly slows down wound healing in cutaneous I/R injuries through increased apoptosis, excessive recruitment of inflammatory cells, and employment of unnecessary pro-inflammatory mechanisms.

In addition, the researchers demonstrated the role of Cl-amidine, a protein-arginine deiminase inhibitor, as effective in normalising exacerbated I/R injury in IL-36Ra mice. Based on these observations, the researchers assert their findings are the first conclusive report of the involvement of IL-36Ra in cutaneous I/R injury.

The team added that they are positive that they have identified a stalwart therapeutic candidate against cutaneous I/R injuries in IL-36Ra. “Our research may lead to the development of therapeutic agents for wound healing of various other refractory skin diseases too,” Tanaka concluded.

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