IL-1β, TNF-α, and IL-10 reduce cell viability and differentially alter biofilm structure and gene expression levels in Staphylococcus aureus USA 300

During infections, S. aureus is exposed to signal molecules from its host, including hormones, cytokines, and chemokines of the immune system, as well as signals from the microbiota that share the same human niches.S. aureus infections cause inflammation and immune modulation signals induction that may be perceived by bacterial biofilms attached to infected tissues.S. aureus is known to respond to catecholamines, steroid hormones, defensins and other host signals.In this work, we analysed whether S. aureus was capable of responding to immunomodulatory signals, such as TNFa, IL-1.(proinflammatory), or IL-10 (anti-inflammatory) cytokines.Biofilm formation and structure, as well as the relative gene expression of global virulence regulators, were evaluated in vitro in S. aureus strain USA300, of human origin.All cytokines decreased the biofilm formation index (BFI) value in a dosedependent manner at concentrations ranging from 0.1 ng/ml to 100 ng/ml.Cytokines exhibit an inhibitory effect on cell viability and induce cytokine-specific structural changes in biofilms, as well as specific alterations in the expression of global regulators' genes.These suggest specific detection and response pathways in S. aureus to each cytokine.