Probiotics and Atopic Dermatitis: An Overview

Irfan A Rather, Vivek K Bajpai, Sanjay Kumar, Jeongheui Lim, Woon K Paek, Yong-Ha Park, Irfan A Rather, Vivek K Bajpai, Sanjay Kumar, Jeongheui Lim, Woon K Paek, Yong-Ha Park

Abstract

Atopic dermatitis (AD) is a common, recurrent, chronic inflammatory skin disease that is a cause of considerable economic and social burden. Its prevalence varies substantially among different countries with an incidence rate proclaimed to reach up to 20% of children in developed countries and continues to escalate in developing nations. This increased rate of incidence has changed the focus of research on AD toward epidemiology, prevention, and treatment. The effects of probiotics in the prevention and treatment of AD remain elusive. However, evidence from different research groups show that probiotics could have positive effect on AD treatment, if any, that depend on multiple factors, such as specific probiotic strains, time of administration (onset time), duration of exposure, and dosage. However, till date we still lack strong evidence to advocate the use of probiotics in the treatment of AD, and questions remain to be answered considering its clinical use in future. Based on updated information, the processes that facilitate the development of AD and the topic of the administration of probiotics are addressed in this review.

Keywords: atopic dermatitis; clinical trials; inflammation; probiotics; skin diseases.

Figures

FIGURE 1
FIGURE 1
Proposed mechanism of probiotics in an animal model of AD. Exposure of atopic skin to a potential allergen enhances the expression of thymic stromal lymphopoietin (TSLP) that is known to activate dendritic cells (DC). Stimulated dendritic cell direct differentiation of naïve T-cell into Th2 cells and Th17 cells which, are known as the mediators of allergic inflammation in skin. Probiotics could inhibit the allergic inflammation by increasing the population of regulatory T cells (Tregs) in the mesenteric lymph nodes of patients. These Tregs could migrate to the site of inflammation and suppress the Th2 and Th17 mediated allergic response or directly reduce the expression of TSLP.

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Source: PubMed

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