Abstract
Atopic dermatitis (AD) is one of the most common skin diseases with inflammation, chronic relapses, and intense pruritus. Its pathogenesis includes genetic susceptibility, an abnormal epidermal lipid barrier, and an increased production of IgE due to immune dysregulation. Recently, AD has been reported to be associated with intestinal inflammation and dysbiosis in human and murine models. Various probiotics are being used to control intestinal dysbiosis and inflammatory reactions. However, it is difficult to predict or determine the therapeutic effects of the probiotics, since it is rare for clinicians to use the probiotics alone to treat AD. It is also difficult to check whether the intestinal inflammation in patients with AD has improved since probiotic treatment. The aim of the present study was to determine whether mice with induced atopic dermatitis had any changes in fecal calprotectin, an indicator of intestinal inflammation, after probiotic administration. Our results showed that the fecal calprotectin levels in mice with induced dermatitis decreased significantly after the administration of probiotics. In addition, epidermal skin lesions were attenuated and inflammatory-related cytokines were downregulated after the administration of probiotics in mice with induced dermatitis. These results suggest that changes in fecal calprotectin levels could be used to assess the effectiveness of a probiotic strain as an adjuvant treatment for AD.
Highlights
Atopic dermatitis (AD) is the most common chronic pruritic inflammatory dermatosis and affects 15–30% of children and 2–10% of adults [1,2,3]
These results suggest that sustained stimulation such as with Ox can induce AD-like skin lesions, which were alleviated by treatment with probiotics
These findings suggest that calprotectin might be an effective indicator of improvements in intestinal inflammation following the administration of probiotics as an adjuvant therapy for atopic patients
Summary
Atopic dermatitis (AD) is the most common chronic pruritic inflammatory dermatosis and affects 15–30% of children and 2–10% of adults [1,2,3]. AD is characterized by complex interactions between genetic and environmental factors, such as skin barrier dysfunction, allergy/immunity, and pruritus [4,5]. Filaggrin is a key protein involved in skin barrier function. Th2 cytokines decrease filaggrin expression by keratinocytes [6,7]. They promote the production of IgE to low doses of allergens, a characteristic commonly observed in AD [8]. Biologics and immunosuppressants targeting immune cells and cytokines have good therapeutic effects on AD, they are not applicable to all patients because of high prices or side effects such as renal toxicity [9,10,11]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
