• Healing skin ischemia-reperfusion injuri

    From ScienceDaily@1:317/3 to All on Mon Nov 8 21:30:44 2021
    Healing skin ischemia-reperfusion injuries with interleukin-36 receptor antagonists
    Researchers from Japan identify the role of interleukin-36 receptor antagonists in healing skin wounds from ischemia-reperfusion injuries

    Date:
    November 8, 2021
    Source:
    Fujita Health University
    Summary:
    Skin wounds from ischemia-reperfusion injuries -- tissue damage
    caused by blood returning to tissues after a period of oxygen
    deprivation -- may not heal appropriately in some patients, owing
    to elusive underlying immunological mechanisms. Scientists from
    Japan have now succeeded in proposing a means to solve this medical
    conundrum by understanding the role of interleukin-36 receptor
    antagonists as they act to inhibit the effects of interleukin-36
    cytokines, which could help identify new therapeutic targets for
    wound healing.



    FULL STORY ========================================================================== Ischemia, which in modern Latin means, "staunching of blood," is a
    medical condition in which the blood supply is cut off to different
    parts of the body.

    In patients who are bed-ridden, ischemia can manifest as pressure
    ulcers. Else, it could be the Raynaud's phenomenon in someone under
    severe stress. This condition can be rescued by blood reperfusion to the affected areas. However, the latter carries the risk of injuries known medically as ischemia-reperfusion (I/R) injuries.


    ========================================================================== Skin-based I/R injuries can be exacerbated by inherited immunological mechanisms, for instance in patients who are otherwise showing signs of
    slow wound healing. To understand the immunological mechanisms underlying
    the development of this condition better, scientists from Japan, building
    on previous studies, decided to narrow down their investigation to interleukin-36 receptor antagonist (IL-36Ra), a protein that plays a
    pivotal immunomodulatory role in wound healing.

    Speaking about the motivation behind their research, Mr. Yoshihito Tanaka
    from Fujita Health University School of Medicine, Japan, who led the team
    of scientists in the investigation, explains, "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. Drawing from experience, IL-36Ra appeared to be a promising candidate for kickstarting
    our investigation." Accordingly, Mr. Tanaka worked with his team to
    understand how deficiency of IL-36Ra affects wound healing in cutaneous
    I/R injuries. For this, the scientists used mice knocked out for
    the receptor. Also, they induced cutaneous I/R injuries in knockout
    and wildtype control mice. Subsequently, they studied corresponding immunological responses in both groups of animals, including the time
    required for wound healing, infiltration of neutrophils/macrophages
    (key immune cells) to the site of the wounds, apoptotic skin cells, and activation of other unwanted immunological defense mechanisms. Their
    findings have been published as a research article in the Journal of
    The European Academy of Dermatology and Venereology.

    The team, comprising Dr. Kazumitsu Sugiura and Dr. Yohei Iwata from
    Fujita Health University School of Medicine, among others, was able to
    pinpoint important results. The scientists found that the absence of
    IL-36Ra, indeed, significantly slows down wound healing in cutaneous
    I/R injuries, through increased apoptosis, or 'suicide' of useful skins
    cells, excessive recruitment of inflammatory cells, and employment of unnecessary proinflammatory mechanisms. Additionally, they demonstrated
    the role of Cl-amidine, a protein- arginine deiminase inhibitor as
    effective in normalizing exacerbated I/R injury in IL-36Ra mice. Based
    on these observations, the scientists assert their findings are the first conclusive report of the involvement of IL-36Ra in cutaneous I/R injury.

    The scientists are positive that they have identified a stalwart
    therapeutic candidate against cutaneous I/R injuries in IL-36Ra. As
    Mr. Tanaka optimistically adds, "Our research may lead to the development
    of therapeutic agents for wound healing of various other refractory
    skin diseases too." The quest for novel therapeutic targets in skin
    wound healing might just have been empowered by these findings of the
    team and the future indeed looks brighter for alleviating the painful
    burden of cutaneous I/R injuries.

    ========================================================================== Story Source: Materials provided by Fujita_Health_University. Note:
    Content may be edited for style and length.


    ========================================================================== Journal Reference:
    1. Yoshihito Tanaka, Yohei Iwata, Kenta Saito, Hidehiko Fukushima,
    Soichiro
    Watanabe, Yurie Hasegawa, Masashi Akiyama, Kazumitsu
    Sugiura. Cutaneous ischemia‐reperfusion injury is exacerbated
    by IL‐36 receptor antagonist deficiency. Journal of the
    European Academy of Dermatology and Venereology, 2021; DOI:
    10.1111/jdv.17767 ==========================================================================

    Link to news story: https://www.sciencedaily.com/releases/2021/11/211108094235.htm

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