Treatment of atopic dermatitis using non-thermal atmospheric plasma in an animal model

Abstract

Cold atmospheric plasma (CAP) has been incorporated into various fields, including promotion of cutaneous wound healing. Atopic dermatitis (AD) is a chronic cutaneous condition characterized by inflammation-induced skin wounds and impaired skin barrier function. To investigate whether CAP may improve AD using an animal model. Dermatophagoides farinae extracts (DFE)-induced murine models of AD were used in this study. The plasma-treated group received a total of 6 CAP treatments during 2 weeks, while the control group did not receive any treatment. Differences in dermatitis severity, transepidermal water loss (TEWL), serum level of immunoglobulin (Ig) E and epidermal thickness were evaluated in both groups. The dermatitis severity was significantly improved by CAP treatment. TEWL was lower in the plasma-treated group compared with the non-treated control group. Serum Ig E dropped significantly after treatment with CAP. Difference in epidermal thickness of the ear skin was not significant between the plasma-treated and non-treated groups. Localized treatment of AD with CAP decreases dermatitis severity, TEWL, and serum Ig E level. These results show CAP’s potentials as a novel therapeutic modality for AD.

A Prospective Randomized Controlled Pilot Study to Assess the Response and Tolerability of Cold Atmospheric Plasma for Rosacea

“…Furthermore, different studies have suggested CAP for the treatment of cancer [37,38]. Atopic dermatitis, psoriasis, and herpes zoster, among others, are further skin diseases in which CAP has been successfully applied [23,[39][40][41][42]. Recently, Karrer et al [43] used a jet plasma device in a prospective, randomized, controlled, split-face trial to assess its safety and efficacy in the treatment of acne vulgaris.…”

Cold Atmospheric Plasma: A Promising and Safe Therapeutic Strategy for Atopic Dermatitis

“…CAP-exposed group showed a more significant decline in DSS on day 17, with a lower TEWL value and the mean epidermal thickness than the AD group. In addition, the level of serum IgE has declined since the seventh day and until the end of the experiment in CAP-exposed group [54]. Meanwhile, CAP increases the expression of HIF-1α in cells, which combines with the promoter region of the MANF gene and enhances the transcription and expression of MANF, thus inhibits inflammation by interacting with the key subunits of NF-κB/p65 [55].…”

Advancements in Cold Atmospheric Plasma for Skin Disease Treatment and Skincare: A Brief Update

“…Researchers have explored the therapeutic effects of atmospheric pressure cold plasma on different mouse models of atopic dermatitis (AD), demonstrating positive outcomes in alleviating skin inflammation, endoplasmic reticulum stress, and oxidative stress [136,137]. Scholars have explored the positive effects of treating AD mice models with non-thermal atmospheric plasma; cold plasma reduced skin cell apoptosis in a mouse model induced with dinitrofluorobenzene (DNFB).…”

“…Furthermore, localized treatment with cold plasma in a mouse model induced by house dust mite extract decreased the severity of dermatitis, transepidermal water loss (TEWL), and serum IgE levels [139]. In another dust mite AD model, plasma inhibited the increase in epidermal thickness recruitment of mast cells and eosinophils and reduced the expression of AD-associated cytokines and chemokines [140].…”

“…In a mouse model induced by 2,4-dinitrofluorobenzene (DNFB), CAP reduced skin cell apoptosis and alleviated skin inflammation, endoplasmic reticulum stress, and oxidative stress, and this anti-inflammatory effect was mediated by MANF expression [193]. In a mouse model induced by house dust mite extract (DFE), local treatment with CAP reduced the severity of dermatitis, transepidermal water loss (TEWL), and serum IgE levels [194]. CAP inhibited the epidermal thickness and the recruitment of mast cells and eosinophils in the AD mouse model induced by house dust mite (HDM) while reducing the expression of AD-related cytokines and chemokines [195].…”