1495 Dimethyl fumarate ameliorates delayed wound healing due to IL-36Ra deficiency through inhibition of NET formation and oxidative stress

Interleukin-36 has been implicated in the pathogenesis of various skin disorders. We previously reported that Il36rn-/- mice revealed delayed wound healing due to excessive recruitment immune cells. In this study, we examined effect dimethyl fumarate (DMF), which is an modulator and inducer antioxidant response, for mice. Full-thickness excisional wounds were produced on back wild was assessed by monitoring macroscopic sizes, numbers infiltrated cells, gene expression inflammatory cytokines. The neutrophil extracellular trap (NET) formation immunofluorescence staining, oxidative stress immunostaining nitrotyrosine. Reactive oxygen species (ROS) measured detection kit. DMF ROS assessed. mRNA levels cytokines using realtime RT-PCR. administration accelerated at 3 7 days after injury. number neutrophils macrophages decreased injury DMF-administered TGF-β IL-1β NET Staining nitrotyrosine vitroexperiments, addition NETs enhanced stress, it suppressed DMF. This study ameliorate IL-36 receptor antagonist deficiency through suppression stress. It speculated production such as may be related increased resulting prolonged healing.