Abstract
Atopic dermatitis (AD) is a common allergic skin disease that is associated with chronic, recurrent eczematous and pruritic lesions at the flexural folds caused by interacting factors related to environmental and immune system changes. AD results in dry skin, and immunoglobulin E-mediated allergic reactions to foods and environmental allergens. While steroids and anti-histamines temporarily relieve the symptoms of AD, the possibility of side effects from pharmacological interventions remains. Despite intensive research, the underlying mechanisms for AD have not been clarified. A study of Staphylococcus aureus (S. aureus) established the role of its toxins in the pathogenesis of AD. Approximately 90% of patients with AD experience S. aureus colonization and up to 50%–60% of the colonizing S. aureus is toxin-producing. Any damage to the protective skin barrier allows for the entry of invading allergens and pathogens that further drive the pathogenesis of AD. Some natural toxins (or their components) that have therapeutic effects on AD have been studied. In addition, recent studies on inflammasomes as one component of the innate immune system have been carried out. Additionally, studies on the close relationship between the activation of inflammasomes and toxins in AD have been reported. This review highlights the literature that discusses the pathogenesis of AD, the role of toxins in AD, and the positive and negative effects of toxins on AD. Lastly, suggestions are made regarding the role of inflammasomes in AD.
Highlights
The chronic inflammatory skin disease, atopic dermatitis (AD), produces eczematous and pruritic lesions at the flexural folds due to interacting factors that are related to environmental and immune system changes [1]
A recent study after exposure to an allergen [44]. This finding suggests a blockade of IL-5 function is applicable to demonstrated that itch signaling was induced by thymic stromal lymphopoietin (TSLP) via sensory neurons [49]. These findings suggest that TSLP has the potential to drive AD pathogenesis in a T helper cell 2 Some (Th2)‐dependent and ‐independent manner while inducing the “itch cycle” in patients aswhich well
Niebuhr et al [176] demonstrated that AD lesional skin exhibited a reduced expression of caspase-1 and nucleotide-binding oligomerization domain receptor protein 3 (NLRP3), and that caspase-1-dependent IL-1β secretion by staphylococcal α-toxin stimulation was impaired in mononuclear cells of AD patients when compared with healthy controls
Summary
The chronic inflammatory skin disease, atopic dermatitis (AD), produces eczematous and pruritic lesions at the flexural folds due to interacting factors that are related to environmental and immune system changes [1]. A recent systematic review showed that 70% of AD patients had S. aureus colonization onespecially their α‐toxin and entero lesional skin, 39% colonization on their non-lesional skin, and 62% on their nose, and meta-regression compared with only 5%–30%. Any damage to severity pathogens effects from pharmacological interventions remains [14]. To solve such problems, current therapies and that further drive. Research have brought about an improvement in clinical symptoms by targeting the specific pathways side effects from pharmaco involved in the pathogenesis of AD. Some studies have reported on the relationship specific pathways involved components) that have thera between inflammasome, one component of the innate immune system, and toxins in AD [16,17,18,19].
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