<p>Allergic contact dermatitis (ACD) is a form of delayed-type hypersensitivity, and it commonly manifests as skin redness, swelling, and itching. Although <i>Ledum palustre</i> var. <i>diversipilosum</i> (LPD) has been utilized in traditional medicine for inflammatory disorders, its preventive potential against ACD has yet to be elucidated. Here, we explored the anti-inflammatory properties of LPD in a murine model of 2,4-dinitrofluorobenzene (DNFB)-induced ACD, with a focus on clinical severity and the modulation of inflammatory signaling molecules. Oral treatment with LPD improved ACD symptoms, as shown by decreases in ear swelling, dermatitis scores, and histopathological changes. LPD also reduced the expression of inflammatory cytokines along with chemokines. Mechanistically, LPD inhibited NF-κB signaling and suppressed NLRP3 inflammasome activation, resulting in lower IL-1β levels and reduced tissue inflammation. Thus, LPD concurrently targets two key pathways driving ACD pathogenesis and exerts anti-inflammatory effects, positioning it as a natural candidate for ACD and other inflammatory skin diseases.</p>

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Ledum palustre var. diversipilosum attenuates DNFB-induced allergic contact dermatitis through regulation of NLRP3 inflammasome/IL-1β signaling

  • Ji-Eun Eom,
  • Young In Kim,
  • Eun Yeong Lim,
  • Hyeon-Ji Song,
  • Ji Yeon Yoo,
  • Gun-Dong Kim,
  • So-Young Lee,
  • Hee Soon Shin

摘要

Allergic contact dermatitis (ACD) is a form of delayed-type hypersensitivity, and it commonly manifests as skin redness, swelling, and itching. Although Ledum palustre var. diversipilosum (LPD) has been utilized in traditional medicine for inflammatory disorders, its preventive potential against ACD has yet to be elucidated. Here, we explored the anti-inflammatory properties of LPD in a murine model of 2,4-dinitrofluorobenzene (DNFB)-induced ACD, with a focus on clinical severity and the modulation of inflammatory signaling molecules. Oral treatment with LPD improved ACD symptoms, as shown by decreases in ear swelling, dermatitis scores, and histopathological changes. LPD also reduced the expression of inflammatory cytokines along with chemokines. Mechanistically, LPD inhibited NF-κB signaling and suppressed NLRP3 inflammasome activation, resulting in lower IL-1β levels and reduced tissue inflammation. Thus, LPD concurrently targets two key pathways driving ACD pathogenesis and exerts anti-inflammatory effects, positioning it as a natural candidate for ACD and other inflammatory skin diseases.