dermatitis, psoriasis, and acnes, considered to arise at least partly from an alteration of these bacterial communities. [2a,4] Staphylococcus epidermidis (S. epidermidis), a permanent member of the human skin microbiota, has been extensively studied because of its prevalence on skin sites and its numerous benefits to hosts. On the one hand, some strains of S. epidermidis have been shown to promote the production of antimicrobial peptides (AMPs) by keratinocytes, [5] and induce T-cell development, [6] resulting in the enhancement of the innate immune protection. The extent and duration of the immune response has also been reported to be controlled by S. epidermidis which diminishes excessive inflammation after injury. [7] On the other hand, diverse molecules, such as phenolsoluble modulins, [8] serine proteases, [9] and nucleobase analogs, [10] can be produced by specific strains of S. epidermidis, leading to the suppression of adjacent microorganism growth. S. epidermidis itself can also secrete AMPs, which have been shown to synergize with the innate immune response to protect the host against pathogens. [11] Therefore, instead of using antibiotics, which have the potential to cause bacterial resistance, bacteriotherapy has been advocated as a promising alternative to prevent skin colonization by pathogenic bacteria. [12] The introduction of S. epidermidis on patients' skin has been shown to significant reduce the colonization by S. aureus and group A Streptococcus. [8-9,11b,13] The short-chain fatty acids produced by S. epidermidis fermentation have been demonstrated to control the growth of Cutibacterium acnes, [11a,14] and of Propionibacterium acnes, [15] which are both important acne triggers.Human beings are colonized by a variety of S. epidermidis strains showing a diversity in pathogenicity. [16] For example, the non biofilm-forming strain ATCC 12228, which lacks the ica operon, [17] is a non-pathogenic commensal. However, some S. epidermidis strains are invasive and are major pathogens in nosocomial infections when they pass through the skin surface and enter the bloodstream via medical devices, for instance. For instance, 47% of coagulase-negative Staphylococci infections are due to S. epidermidis strains which often are methicillin-and multidrug-resistant. [18] Genomic analysis of both commensal and nosocomial strains demonstrate that they share approximately 80% of their genomes, with the 20%
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