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Cutibacterium acnes phylotypes diversity loss: a trigger for skin inflammatory process
Author(s) -
Dagnelie M.A.,
Corvec S.,
SaintJean M.,
Nguyen J.M.,
Khammari A.,
Dréno B.
Publication year - 2019
Publication title -
journal of the european academy of dermatology and venereology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.655
H-Index - 107
eISSN - 1468-3083
pISSN - 0926-9959
DOI - 10.1111/jdv.15795
Subject(s) - phylotype , acne , innate immune system , medicine , immune system , immunology , biology , dermatology , gene , 16s ribosomal rna , genetics
Background Acne has long been understood as a multifactorial chronic inflammatory disease of the pilosebaceous follicle, where Cutibacterium acnes (subdivided into six main phylotypes) is a crucial factor. In parallel, the loss of microbial diversity among the skin commensal communities has recently been shown as often accompanied by inflammatory skin disorders. Objective This study investigated the association of C. acnes phylotype diversity loss and the impact on Innate Immune System (IIS) activation. Methods The IIS response of skin after incubation with phylotypes IA1, II or III individually and with the combination of IA1 + II + III phylotypes, was studied in an in vitro skin explant system. The inflammatory response was monitored by immunohistochemistry and ELISA assays, targeting a selection of Innate Immune Markers (IIMs) (IL‐6, IL‐8, IL‐10, IL‐17, TGF‐β). Results IIMs were significantly upregulated in skin when being incubated with phylotype IA1 alone compared with the combination IA1 + II + III. In parallel, ELISA assays confirmed these results in supernatants for IL‐17, IL‐8 and IL‐10. Conclusion We identify the loss of C. acnes phylotype diversity as a trigger for IIS activation, leading to cutaneous inflammation. These innovative data underline the possibility to set up new approaches to treat acne. Indeed, maintaining the balance between the different phylotypes of C. acnes may be an interesting target for the development of drugs.

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