Abstract
Atopic dermatitis (AD) is a biphasic inflammatory skin disease that is provoked by epidermal barrier defects, immune dysregulation, and increased skin infections. Previously, we have demonstrated that bvPLA2 evoked immune tolerance by inducing regulatory T cells (Treg), and thus alleviated Th2 dominant allergic asthma in mice. Here, we would like to determine whether treatment with bvPLA2 exacerbates the AD-like allergic inflammations induced by house dust mite extract (DFE) in a murine model. Epidermal thickness, immune cell infiltration, serum immunoglobulin, and cytokines were measured. Ear swelling, skin lesions, and the levels of total serum IgE and Th1/Th2 cytokines were elevated in DFE/DNCB-induced AD mice. Topical application of bvPLA2 elicited significant suppression of the increased AD symptoms, including ear thickness, serum IgE concentration, inflammatory cytokines, and histological changes. Furthermore, bvPLA2 treatment inhibited mast cell infiltration into the ear. On the other hand, Treg cell depletion abolished the anti-atopic effects of bvPLA2, suggesting that the effects of bvPLA2 depend on the existence of Tregs. Taken together, the results revealed that topical exposure to bvPLA2 aggravated atopic skin inflammation, suggesting that bvPLA2 might be a candidate for the treatment of AD.
Highlights
Atopic dermatitis (AD) is a common chronic and recurrent inflammatory skin disease that results from dysregulated immune responses due to excessive stimulation by external antigens [1].The prevalence of AD has significantly increased in recent years, and it affects approximately1%–3% of adults and up to 20% of children [2]
We investigated the effects of bvPLA2 on the alleviation of Dermatophagoides farinae extract (DFE)/DNCB-induced AD-like symptoms
We previously reported that bvPLA2 can induce Foxp3-expressing CD4+ regulatory T cells
Summary
Atopic dermatitis (AD) is a common chronic and recurrent inflammatory skin disease that results from dysregulated immune responses due to excessive stimulation by external antigens [1]. AD patients exhibit epidermal hyperplasia and accumulations of mast cells and Th2 cytokines [6,7]. Many cases of AD are treated with anti-inflammatory agents that modulate Th1 and Th2 responses and the IgE concentration. Our recent study demonstrated that bvPLA2 causes immune tolerance by increasing the population of CD4+ Foxp3+ regulatory T cells (Tregs) in cisplatin-induced nephrotoxicity and allergic asthma models [17,18]. We hypothesized that bvPLA2 might be a candidate anti-inflammatory agent for AD treatment. In addition to the infiltration of mast cells, epidermal hyperplasia is reduced upon bvPLA2 treatment in AD mice. This study proposes that bvPLA2 is a potential novel therapeutic agent for the treatment of AD patients
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