490 CLINICAL REPORT
ActaDV ActaDV Advances in dermatology and venereology Acta Dermato-Venereologica
Propionibacterium acnes Abundance Correlates Inversely with Staphylococcus aureus: Data from Atopic Dermatitis Skin Microbiome
Wojciech FRANCUZIK 1, Kristin FRANKE 1, Ralf R. SCHUMANN 2, Guido HEINE 1 and Margitta WORM 1
1
Department of Dermatology, Venereology and Allergology, and 2 Institute for Microbiology and Hygiene, Charité Universitätsmedizin Berlin, Berlin, Germany
The microbiome may influence disease severity in atopic dermatitis. The skin of atopic dermatitis patients and healthy individuals was sampled in a standardized manner and the microbial composition analysed using next-generation sequencing. Optical density measurements were used to investigate bacterial growth under defined conditions in vitro. Lesional skin from patients with atopic dermatitis had a higher abundance of Staphylococcus aureus and reduced quantities of Propionibacterium acnes and Lawsonella clevelandensis compared with non-lesional skin. The abundance of P. acnes correlated negatively with that of S. aureus( ρ = – 0.6501, p < 0.0001). Fermentation products of P. acnes inhibited the growth of S. aureus and S. epidermidis. Serum from patients with atopic dermatitis inhibited the growth of S. aureus to a greater extent than did serum from healthy individuals. These results suggest that selective modification of the skin microbiome could potentially be used as a therapeutic strategy in atopic dermatitis.
Key words: P. acnes; atopic dermatitis; S. aureus; microbiota, high-throughput nucleotide sequencing; skin; eczema.
Accepted Jan 29, 2018; Epub ahead of print Jan 30, 2018 Acta Derm Venereol 2018; 98: 490 – 495.
Corr: Margitta Worm, Department of Dermatology, Venereology and Allergology, Charité Universitätsmedizin Berlin, Charitéplatz 1, DE-10117, Berlin, Germany. E-mail: margitta. worm @ charite. de
Atopic dermatitis( AD) is a chronic, pruritic inflammatory skin disease with an estimated prevalence of 10 – 20 % among children in Western countries and 2 – 3 % among adults( 1). A genetically determined defect in epidermal function is thought to be the initial mechanism in the pathogenesis of AD( 2). This barrier defect results in increased water loss, xerosis and reactivity of immune cells to exogenous antigens, such as pollen and microbial flora. The ensuing immune reaction in the skin leads to pruritus and scratching, which further promote inflammation. Lesional overgrowth with Staphylococcus aureus has been described in several reports. S. aureus is a well-known pathogen that can increase disease severity( 3) and has been found to be more frequent in patients with AD than in healthy individuals( 4).
The Human Microbiome Project described the composition of the healthy skin microflora( 5), and skin microbiome dysregulation has been reported previously in patients with AD( 6, 7). Mechanisms that either promote or depend on changes to the microbiome are currently of high scientific interest. It has been shown that the commensal skin microbiome impacts on local and systemic immunity( 8). The lesional overgrowth of S. aureus correlates with AD flare-ups( 9). S. epidermidis, which is considered a harmless skin commensal, promotes an innate immune response( 10, 11) and, moreover, inhibits the growth of S. aureus and Propionibacterium acnes( 12).
The skin microbiome in healthy individuals and patients with AD with lesions in various anatomical sites was studied using an unbiased approach in order to determine whether a common form of microbial dysregulation is present in patients with AD. By analysing how skin bacteria interact with each other, the aim of this study is to elucidate the underlying mechanisms of AD and provide a basis for the development of novel therapeutic strategies for this disease.
METHODS Patient recruitment and sampling
Ethical approval for this single-centre research study was provided by the Charité Ethical Committee( EA1 / 194 / 14). After obtaining written informed consent, patients with AD and healthy individuals( 7 in each group) were included in the study. All procedures were performed in accordance with the Declaration of Helsinki( 13). The participants were recruited from the outpatient clinic of the Department of Dermatology Venereology and Allergology. The inclusion criteria for the AD group( modified from( 9)) comprised a diagnosis of child-onset AD according to the criteria of Hanifin & Rajka( 14); abstaining from the use of topical corticosteroids, skin disinfectants or antibiotics for at least 4 weeks; and avoiding skin washing for 12 h prior to sampling. All participants were male, between 18 and 60 years of age, and were included after a thorough examination at the Comprehensive Allergy Center Charité.
The control group was composed of non-atopic, healthy volunteers with no personal or family history of allergic rhinitis, allergic asthma, or atopic dermatitis, with negative standard prick test results, and normal serum IgE concentrations. To allow for naïve microbial skin colonization, volunteers were excluded if they had used skin disinfectants, topical corticosteroids or antibiotics in the 4 weeks prior to sampling.
Sampling was performed according to the protocol by Oh( 15). However, we enlarged the sampling area to increase DNA concentrations in the final samples. Catch-All swabs( Epicentre, Madison, WI, USA) were moisturized with DNAse-free water and used in 3 strictly defined locations( antecubital fossa 40 cm 2, interscapular region 40 cm 2 and retroauricular region 10 cm 2). DNA was extracted using the PowerSoil DNA Isolation Kit( MO BIO Laboratories, Inc., Carlsbad, CA, USA), quantified using a BioPhotometer( Eppendorf AG, Hamburg, Germany) and confirmed by conventional PCR( using 341F: CCTACgggAggCAgCAg doi: 10.2340 / 00015555-2896 Acta Derm Venereol 2018; 98: 490 – 495
This is an open access article under the CC BY-NC license. www. medicaljournals. se / acta Journal Compilation © 2018 Acta Dermato-Venereologica.