Abstract
Recent reports have shown the immunomodulatory effect of heat-killed lactic acid bacteria. Atopic dermatitis (AD) is an allergic skin disease, caused by immune dysregulation among other factors. The aim of this study was to assess the effect of heat-killed Enterococcus faecalis EF-2001 (EF-2001) on AD. We established an in vivo AD model by repeated local exposure of Dermatophagoides farinae extract (DFE; house dust mite extract) and 2,4-dinitrochlorobenzene (DNCB) to the ears of mice. After oral administration of EF-2001 for four weeks, the epidermal and dermal ear thickness, mast cell infiltration, and serum immunoglobulin levels were measured. In addition, the gene expression levels of pathogenic cytokines in the ears, lymph nodes, and splenocytes were assayed. EF-2001 attenuated AD symptoms based on the ear thickness, histopathological analysis, and serum immunoglobulin levels. Moreover, EF-2001 decreased the DFE/DNCB-induced expression of various pathogenic cytokines in the ears, lymph nodes, and splenocytes. These results suggest that EF-2001 has therapeutic potential in the treatment of AD owing to its immunomodulatory effects.
Highlights
Many probiotic bacteria have been described as promising agents for the treatment and prevention of atopic dermatitis (AD) by influencing the host’s immune system [1,2]
It has been suggested that administration of probiotics may have preventive and/or therapeutic potential in AD [1,2]
There are case reports of complications resulting from specific bacteria therapy; this suggests that revising probiotic safety aspects may be warranted [19,20,21]
Summary
Many probiotic bacteria have been described as promising agents for the treatment and prevention of atopic dermatitis (AD) by influencing the host’s immune system [1,2]. Most of these bacteria are lactic acid bacteria, which form part of the healthy human microbiota. Recent research findings have provided insight into the complex pathogenic mechanisms involved in AD [4]. The pathogenesis of AD involves immune dysregulation [5], marked epidermal hyperplasia in chronic lesional skin [6], and increased susceptibility to infections [7]. The exact pathogenesis of AD is not yet completely understood, it is generally characterized by excessive
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