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Oral administration of Faecalibacterium prausnitzii and Akkermansia muciniphila strains from humans improves atopic dermatitis symptoms in DNCB induced NC/Nga mice
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Oral administration of Faecalibacterium prausnitzii and Akkermansia muciniphila strains from humans improves atopic dermatitis symptoms in DNCB induced NC/Nga mice
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Journal Article
Oral administration of Faecalibacterium prausnitzii and Akkermansia muciniphila strains from humans improves atopic dermatitis symptoms in DNCB induced NC/Nga mice
2022
Overview
Atopic dermatitis (AD) is a common inflammatory skin disease, and its pathogenesis is closely associated with microbial homeostasis in the gut, namely the gut-skin axis. Particularly, recent metagenomics studies revealed that the abundance of two major bacterial species in the gut,
Faecalibacterium prausnitzii
and
Akkermansia muciniphila
, may play a critical role in the pathogenesis of AD, but the effect of these species in AD has not yet been elucidated. To evaluate the potential beneficial effect of
F. prausnitzii
or
A. muciniphila
in AD, we conducted an animal model study where
F. prausnitzii
EB-FPDK11 or
A. muciniphila
EB-AMDK19, isolated from humans, was orally administered to 2,5-dinitrochlorobenzene (DNCB)-induced AD models using NC/Nga mice at a daily dose of 10
8
CFUs/mouse for six weeks. As a result, the administration of each strain of
F. prausnitzii
and
A. muciniphila
improved AD-related markers, such as dermatitis score, scratching behavior, and serum immunoglobulin E level. Also, the
F. prausnitzii
and
A. muciniphila
treatments decreased the level of thymic stromal lymphopoietin (TSLP), triggering the production of T helper (Th) 2 cytokines, and improved the imbalance between the Th1 and Th2 immune responses induced by DNCB. Meanwhile, the oral administration of the bacteria enhanced the production of filaggrin in the skin and ZO-1 in the gut barrier, leading to the recovery of functions. Taken together, our findings suggest that
F. prausnitzii
EB-FPDK11 and
A. muciniphila
EB-AMDK19 have a therapeutic potential in AD, which should be verified in humans.
Publisher
Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio
Subject
