Inflammatory cytokines and biofilm production sustain Staphylococcus aureus outgrowth and persistence: a pivotal interplay in the pathogenesis of Atopic Dermatitis

• DOI: 10.1038/s41598-018-27421-1
• Publication Date: 2018-06-18T11:58:29Z
• Authors: E. G. Di Domenico; I. Cavallo; V. Bordignon; G. Prignano; I. Sperduti; A. Gurtner; E. Trento; L. Toma; F. Pimpinelli; B. Capitanio; F. Ensoli
• Keywords: Coagulase; Male; Staphylococcus aureus; 0303 health sciences; Infant; Biofilm; atopic dermatitis; inflammatory cytokines; Microbial Sensitivity Tests; Severity of Illness Index; Article; Dermatitis, Atopic; 3. Good health; 03 medical and health sciences; Anti-Infective Agents; Biofilms; Child, Preschool; Drug Resistance, Bacterial; Cytokines; Humans; Female; Inflammation Mediators; Child; Oxacillin; Skin

AbstractIndividuals with Atopic dermatitis (AD) are highly susceptible toStaphylococcus aureuscolonization. However, the mechanisms driving this process as well as the impact ofS. aureusin AD pathogenesis are still incompletely understood. In this study, we analysed the role of biofilm in sustainingS. aureuschronic persistence and its impact on AD severity. Further we explored whether key inflammatory cytokines overexpressed in AD might provide a selective advantage toS. aureus. Results show that the strength of biofilm production byS. aureuscorrelated with the severity of the skin lesion, being significantly higher (P < 0.01) in patients with a more severe form of the disease as compared to those individuals with mild AD. Additionally, interleukin (IL)-β and interferon γ (IFN-γ), but not interleukin (IL)-6, induced a concentration-dependent increase ofS. aureusgrowth. This effect was not observed with coagulase-negative staphylococci isolated from the skin of AD patients. These findings indicate that inflammatory cytokines such as IL1-β and IFN-γ, can selectively promoteS. aureusoutgrowth, thus subverting the composition of the healthy skin microbiome. Moreover, biofilm production byS. aureusplays a relevant role in further supporting chronic colonization and disease severity, while providing an increased tolerance to antimicrobials.