Understanding the control of the optical and plasmonic properties of unique nanosystems—gold nanostars—both experimentally and theoretically permits superior design and fabrication for biomedical applications. Here, we present a new, surfactant-free synthesis method of biocompatible gold nanostars with adjustable geometry such that the plasmon band can be tuned into the near-infrared region ‘tissue diagnostic window’, which is most suitable for in vivo imaging. Theoretical modelling was performed for multiple-branched 3D nanostars and yielded absorption spectra in good agreement with experimental results. The plasmon band shift was attributed to variations in branch aspect ratio, and the plasmon band intensifies with increasing branch number, branch length, and overall star size. Nanostars showed an extremely strong two-photon photoluminescence (TPL) process. The TPL imaging of wheat-germ agglutinin (WGA) functionalized nanostars on BT549 breast cancer cells and of PEGylated nanostars circulating in the vasculature, examined through a dorsal window chamber in vivo in laboratory mouse studies, demonstrated that gold nanostars can serve as an efficient contrast agent for biological imaging applications.

Aim To explore the involvement of TLR5 in pulp inflammation and to examine the effects of TLR5 activation with its ligand, FlaB protein, on pro‐inflammatory gene expression. Methodology TLR5 expression in dental pulp tissues and human dental pulp cells (hDPCs) were determined by immunohistochemistry, immunocytochemistry, Western blots and RT‐PCR analyses. To examine the role of TLR5, hDPCs were treated with recombinant FlaB protein (500 ng mL−1) to activate the receptor or with a small interfering RNA against TLR5 (si‐TLR5) to downregulate the receptor. After exposure to FlaB, the expression of inflammation‐related proteins was screened using a protein array kit. Western blots or qRT‐PCR analyses were performed to identify changes in the expression of uPA (urokinase plasminogen activator), TIMPs (tissue inhibitor of metalloproteinases), and IL‐6 and to determine their signalling pathways. Statistical analysis was performed using one‐way analysis of variance (anova) with Tukey post hoc test; P < 0.05 was considered statistically significant. Result TLR5 expression was identified in pulp tissues and hDPCs. In the protein array analysis, treatment with FlaB significantly increased uPA expression (P < 0.01) and significantly decreased TIMP1/4 (P < 0.05). FlaB treatment also significantly increased expression of the inflammatory marker IL‐6 (P < 0.01). FlaB treatment increased phosphorylation of the NF‐κB p65 subunit, JNK, p38 and ERK. Chemical inhibitors of NF‐κB (Bay11‐7082), p38 (SB202190) or ERK (U0126) decreased the FlaB induction of uPA expression. Downregulation of TLR5 expression by siRNA decreased the FlaB induction of uPA protein and p65 phosphorylation. Conclusion TLR5 activation with FlaB treatment induced the expression of uPA via the NF‐κB and MAPK signalling pathways. Flagellin‐bearing oral bacteria may cause pulp inflammation through TLR5. The findings provide new clues to control pulpal diseases by targeting TLR5 signalling pathways.

No abstract