Staphylococcus epidermidis protease EcpA can be a deleterious component of the skin microbiome in atopic dermatitis - 04/03/21
Abstract |
Background |
Staphylococcus aureus and Staphylococcus epidermidis are the most abundant bacteria found on the skin of patients with atopic dermatitis (AD). S aureus is known to exacerbate AD, whereas S epidermidis has been considered a beneficial commensal organism.
Objective |
In this study, we hypothesized that S epidermidis could promote skin damage in AD by the production of a protease that damages the epidermal barrier.
Methods |
The protease activity of S epidermidis isolates was compared with that of other staphylococcal species. The capacity of S epidermidis to degrade the barrier and induce inflammation was examined by using human keratinocyte tissue culture and mouse models. Skin swabs from atopic and healthy adult subjects were analyzed for the presence of S epidermidis genomic DNA and mRNA.
Results |
S epidermidis strains were observed to produce strong cysteine protease activity when grown at high density. The enzyme responsible for this activity was identified as EcpA, a cysteine protease under quorum sensing control. EcpA was shown to degrade desmoglein-1 and LL-37 in vitro, disrupt the physical barrier, and induce skin inflammation in mice. The abundance of S epidermidis and expression of ecpA mRNA were increased on the skin of some patients with AD, and this correlated with disease severity. Another commensal skin bacterial species, Staphylococcus hominis, can inhibit EcpA production by S epidermidis.
Conclusion |
S epidermidis has commonly been regarded as a beneficial skin microbe, whereas S aureus has been considered deleterious. This study suggests that the overabundance of S epidermidis found on some atopic patients can act similarly to S aureus and damage the skin by expression of a cysteine protease.
Le texte complet de cet article est disponible en PDF.Graphical abstract |
Key words : Atopic dermatitis, microbiome, dysbiosis, Staphylococcus epidermidis, protease, skin, epidermal barrier, inflammation, cytokine
Abbreviations used : AD, agr, AIP, AMP, CFU, CoNS, DSG-1, EcpA, IVL, HEK, PSM, qPCR, TEWL, TSB, WT
Plan
| This work was funded by National Institutes of Health grants R01 AR076082, R37 AI052453, and U19 AI117673. Postdoctoral fellowship support for L. Cau was provided by SILAB. A. R. Horswill was supported by a Merit Award (BX002711) from the US Department of Veteran Affairs. |
|
| Disclosure of potential conflict of interest: R. L. Gallo is a cofounder, scientific advisor, and consultant of MatriSys Biosciences and has equity in the company; in addition, he receives income from and has equity in Sente. The rest of the authors declare that they have no relevant conflicts of interest. |
Vol 147 - N° 3
P. 955 - mars 2021 Retour au numéro
Article précédent
- Single-cell transcriptomic analysis reveals key immune cell phenotypes in the lungs of patients with asthma exacerbation
- Hui Li, Huaqi Wang, Leon Sokulsky, Shaoxia Liu, Rui Yang, Xiaojie Liu, Lujia Zhou, Juan Li, Chun Huang, Fangfang Li, Xu Lei, Hongxia Jia, Jiuling Cheng, Fuguang Li, Ming Yang, Guojun Zhang
- Association of frequent moisturizer use in early infancy with the development of food allergy
- Michael R. Perkin, Kirsty Logan, Tom Marrs, Suzana Radulovic, Joanna Craven, Robert J. Boyle, Joanne R. Chalmers, Hywel C. Williams, Serge A. Versteeg, Ronald van Ree, Gideon Lack, Carsten Flohr, EAT Study Team, Louise Young, Victoria Offord, Mary DeSousa, Jason Cullen, Katherine Taylor, Anna Tseng, Bunmi Raji, Sarah Byrom, Gillian Regis, Charlie Bigwood, Charlotte Stedman, Sharon Tonner, Emily Banks, Yasmin Kahnum, Rachel Babic, Ben Stockwell, Erin Thompson, Lorna Wheatley, Devi Patkunam, Kerry Richards, Ewa Pietraszewicz, Alick Stephens, Asha Sudra, Victor Turcanu
Bienvenue sur EM-consulte, la référence des professionnels de santé.
L’accès au texte intégral de cet article nécessite un abonnement.
Déjà abonné à cette revue ?