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Bacterial infections caused by implanted/interventional medical devices have become the main component of health care-associated infection (HAT)，threatening the health of patients and causing huge economic losses. Construction of antibacterial coating on the surface of medical devices is one of the most effective and practical methods to prevent and inhibit HAL Light-mediated antibacterial coatings，which use light irradiation to inactivate bacteria? are flexible and controllable? and won't cause bacterial resistance. Those advantages have attracted extensive attention. In this paper ? the mechanism ? research progress and development trend of lightmediated antibacterial coatings were summarized. [ABSTRACT FROM AUTHOR]

Objective To investigate the effect and mechanism of HBV 一 stimulated HTR8 一 S/Vneo mitochondrial antiviral signaling protein (MAVS) signaling pathway on the immune response of peripheral blood mononuclear cell (PBMC) to hepatitis B vaccine. Methods The HTR8 - S/Vneo were co 一 incubated with serum of HBV - DNA positive patients. MAVS siRNA transfection was hereby applied for silencing of MAVS and MAVS plasmid transfection was applied for overexpression of MAVS in HTR8 一 S/Vneo. We then cocultured them with human immune cells assembly PBMC and subsequently stimulated with hepatitis B vaccine. The mRNA and protein expression levels of MAVS, NF - kB, pNF - kB, IRF3 and pIRF3 in HTR8 一 S/Vneo were detected by reverse transcription 一 quantitative real 一 time PCR (RT 一 qPCR) and flow cytometry (FCM). The levels of IL - 2, IL - 6, IFN 一 p and IL 一 17 were detected by enzyme - linked immunosorbent assay (ELISA), and the proportion of CD4+ T cell were detected by flow cytometry. The data were analyzed for t test. Results HBV down 一 regulated the mRNA expression levels of MAVS, NF - kB, IRF3 (£ 二 6. 66, P 二 0. 003; £ 二 14. 18, P < 0. 001; £ 二 3. 70, P 二 0. 021) and the protein expression levels of MAVS, NF - kB, pNF - kB(£ 二 3. 42, P = 0. 042; £ 二 4. 23, P = 0. 013; £ 二 4. 86, P - 0. 008), and inhibited the production of IFN - p(£ 二 9. 83, P = 0. 010). Silencing MAVS down 一 regulated the mRNA and protein expression of MAVS(£ 二 31. 20, P < 0. 001; £ 二 6. 53, P = 0. 023), inhibited the expression of IFN - p(£ 二 5. 46, P =0. 032), and reduced the proportion of CD4+ T cells in PBMC(£ 二 9. 07, P = 0. 001). Overexpression of MAVS induced IFN 一 B production(£ 二一 34. 26, P < 0. 001; t - -5. 11, P = 0, 036), but the proportion of CD4 * T cells did not show significant effect (/二 一 0. 73, P 二 0. 506). Conclusion HBV can inhibit the MAVS signaling pathway in HTR8 一 S/Vneo. Overexpression of MAVS could promote the immune response to hepatitis B vaccine in PBMC. [ABSTRACT FROM AUTHOR]