Heat-Killed Enterococcus faecalis EF-2001 Ameliorates Atopic Dermatitis in a Murine Model

Nutrients. 2016 Mar 5;8(3):146. doi: 10.3390/nu8030146.

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.

Keywords: atopic dermatitis; heat-killed Enterococcus faecalis EF-2001; immunomodulatory; lactic acid bacteria; pathogenic cytokines.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cytokines / immunology
  • Cytokines / metabolism
  • Dermatitis, Atopic / immunology
  • Dermatitis, Atopic / metabolism
  • Dermatitis, Atopic / microbiology
  • Dermatitis, Atopic / therapy*
  • Disease Models, Animal
  • Enterococcus faecalis / immunology*
  • Female
  • Hot Temperature*
  • Inflammation Mediators / immunology
  • Inflammation Mediators / metabolism
  • Mice, Inbred BALB C
  • Probiotics*
  • Skin / immunology*
  • Skin / metabolism
  • Skin / microbiology
  • Skin / pathology
  • Time Factors

Substances

  • Cytokines
  • Inflammation Mediators