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A multistrain probiotic formulation attenuates skin symptoms of atopic dermatitis in a mouse model through the generation of CD4 + Foxp3 + T cells.
BACKGROUND: Atopic dermatitis (AD) is characterized by chronic inflammation of the skin. AD develops mainly in infants and young children. It induces skin disorders and signals the initiation of the allergic march including allergic asthma and rhinitis. Probiotics modify intestinal microbial populations in a beneficial way for human and animal hosts by reducing inflammatory cytokines.
OBJECTIVE: As a result of their immunomodulatory properties, probiotics have been considered a promising therapeutic option for the prevention and treatment of AD.
DESIGN: In this study, we examined the effects of GI7, a potential probiotic mixture consisting of seven strains of bifidobacteria and lactic acid bacteria, on AD in a mouse model.
RESULTS: Administration of GI7 for 8 weeks reduced AD-like skin lesions and induced changes in the levels of serum markers such as immunoglobulin E and cytokines related to T helper (Th)1 and Th2 cells, and in skin barrier genes. Alleviation of AD seems to be associated with GI7-induced generation of CD4+ Foxp3+ regulatory T cells.
CONCLUSIONS: The probiotic mixture may have potential to improve symptoms of AD.
OBJECTIVE: As a result of their immunomodulatory properties, probiotics have been considered a promising therapeutic option for the prevention and treatment of AD.
DESIGN: In this study, we examined the effects of GI7, a potential probiotic mixture consisting of seven strains of bifidobacteria and lactic acid bacteria, on AD in a mouse model.
RESULTS: Administration of GI7 for 8 weeks reduced AD-like skin lesions and induced changes in the levels of serum markers such as immunoglobulin E and cytokines related to T helper (Th)1 and Th2 cells, and in skin barrier genes. Alleviation of AD seems to be associated with GI7-induced generation of CD4+ Foxp3+ regulatory T cells.
CONCLUSIONS: The probiotic mixture may have potential to improve symptoms of AD.
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