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. 2020 Jul 7;12(31):34610–34619. doi: 10.1021/acsami.0c08592

Figure 7.

Figure 7

Growth of HGF cells on NIR-irradiated (1 W/cm2, 808 nm), PDA-NP-coated (200 μg/cm2) titanium surfaces after a challenge by S. aureus ATCC12600 in a late postoperative infection model in which a protective keratinocyte seal is present. (A) Schematics of the late postoperative infection model (A1), in which an HGF layer on an implant surface in the presence of a protective keratinocyte seal is challenged with S. aureus ATCC12600 (1 ×103 CFU/cm2) and irradiated, followed by 24 h of further growth of the HGF layer. Fluorescence images (A2) of DAPI/TRITC-stained HGF cells further grown after an S. aureus challenge, in the absence (0 min) and in presence of irradiation (samples immersed in 10 μL of DMEM-HG medium). Red fluorescence indicates skeleton spreading, and blue fluorescence indicates HGF nuclei. The scale bar represents 100 μm. (B) Surface coverage by adhering HGF on PDA-NP-coated titanium surfaces after a staphylococcal challenge in the absence (0 min) and presence of NIR irradiation while immersed in different DMEM-HG volumes. (C) Same as (B) but for the number of adhering HGFs per unit area. Error bars denote SEM over three experiments with separately cultured cells. * Denotes a significant difference upon NIR irradiation (p < 0.05), compared with staphylococcal contamination in the absence of NIR irradiation. # Denotes similarity, i.e., no significant difference in the presence of staphylococcal contamination and after NIR irradiation (p > 0.05), compared with the absence of staphylococcal contamination.