Fig. 4
Human nasal mucus-derived S. epidermidis induces interferon (IFN)-λ production and suppresses infection spread in influenza A virus (IAV)-infected mice. a Schematic of the mouse model experimental design. The native microbiome of the C57BL/6J mice was depleted with an antibiotic regimen prior to inoculation. The mice (N = 4) were inoculated with S. epidermidis (3.2 × 106 CFU/30 μl PBS) and/or with IAV (213 PFU) at the indicated time points. b Mean body weight of S epidermidis-inoculated mice with or without IAV infection was measured. IAV PA mRNA levels in the mouse lung tissue (c) were assessed at 7 days post-infection (dpi) and hematoxylin and eosin (H&E)-stained micrographs (d) were also generated from lung sections obtained at 7 dpi. B6 mice were inoculated with human nasal mucus-derived S. epidermidis and non-pathogenic laboratory S. epidermidis 12228 before IAV infection and H&E-stained micrographs (e) were also generated from lung sections obtained at 7 dpi. Micrographs shown are representative of lung sections from four mice. The micrographs were used to assess inflammation and tissue damage and to calculate a histological score. f S. epidermidis CFUs in the NAL and BAL fluid samples were determined at 7 dpi. g IFN-λ2/3 mRNA levels in mouse nasal mucosa and lung tissue at 7 dpi were measured using real-time PCR. h Concentrations of mouse NAL and BAL fluid samples were compared to secreted IFN-λ concentrations using ELISA. Real-time PCR, plaque assay, and ELISA results are presented as mean ± SD from four independent experiments. *p < 0.05 compared with mice infected with IAV alone