A sandwich-structured multifunctional platform based on self-assembled Ti3C2Tx@Au NPs films, antibiotics, and silent region SERS probe for the capture, determination, and drug resistance analysis of Gram-positive bacteria.

A multifunctional surface-enhanced Raman scattering (SERS) platform integrating sensitive detection and drug resistance analysis was developed for Gram-positive bacteria. The substrate was based on self-assembled Ti3C2Tx@Au NPs films and capture molecule phytic acid (IP6) to achieve specific capture of Gram-positive bacteria and different bacteria were analyzed by fingerprint signal. It had advantages of good stability and homogeneity (RSD = 8.88%). The detection limit (LOD) was 102 CFU/mL for Staphylococcus aureus and 103 CFU/mL for MRSA, respectively. A sandwich structure was formed on the capture substrate by signal labels prepared by antibiotics (penicillin G and vancomycin) and non-interference SERS probe molecules (4-mercaptobenzonitrile (2223 cm-1) and 2-amino-4-cyanopyridine (2240 cm-1)) to improve sensitivity. The LOD of Au NPs@4-MBN@PG to S. aureus and Au NPs@AMCP@Van to MRSA and S. aureus were all improved to 10 CFU/mL, with a wide dynamic linear range from 108 to 10 CFU/mL (R2 ≥ 0.992). The SERS platform can analyze the drug resistance of drug-resistant bacteria. Au NPs@4-MBN@PG was added to the substrate and captured MRSA to compare the SERS spectra of 4-MBN. The intensity inhomogeneity of 4-MBN at the same concentrations of MRSA and the nonlinearity at the different concentrations of MRSA revealed that MRSA was resistant to PG. Finally, the SERS platform achieved the determination of MRSA in blood. Therefore, this SERS platform has great significance for the determination and analysis of Gram-positive bacteria.

Nb2C MXene self-assembled Au nanoparticles simultaneously based on electromagnetic enhancement and charge transfer for surface enhanced Raman scattering.

Recent years, two-dimensional transition metal carbonitrides (MXene) have attracted much attention in the field of surface-enhanced Raman scattering (SERS). However, the relatively low enhancement of MXene is a major challenge. Herein, Nb2C-Au NPs nanocomposites were prepared by electrostatic self-assembly method, which have a synergistically conjugated SERS effect. The EM hot spots of Nb2C-Au NPs are significantly enlarged and expanded, while the surface Fermi level is decreased. This synergistic effect could improve the SERS performance of the system. Consequently, for the dye molecules CV and MeB, the detection limits reach 10-10 M and 10-9 M, respectively, while for biomolecule adenine, the detection limit is as low as 5 × 10-8 M. The results also show the good concentration-dependent linearity, uniformity, reproducibility and stability of SERS substrate. Nb2C-Au NPs could be a fast, sensitive and stable SERS platform for label-free and non-destructive detection. This work may expand the application of MXene based materials in the field of SERS.

MicroRNA-206 promotes lipopolysaccharide-induced inflammation injury via regulation of IRAK1 in MRC-5 cells.

BACKGROUND: MicroRNAs (miRNAs) have been reported to play crucial role in the airway inflammatory diseases. However, the involvement of miR-206 in airway inflammatory diseases is still uninvestigated. The study aimed to explore the effect of miR-206 on lipopolysaccharide (LPS)-induced inflammation injury in MRC-5 cells, and point out a potential relevance for chronic obstructive pulmonary disease (COPD). METHODS: LPS was utilized to expose MRC-5 cells, then cell viability, cell migration, apoptosis, apoptosis-associated factors, as well as the concentrations and protein levels of IL-6 and IL-8 were explored. After transfected with miR-206 mimic and inhibitor, above parameters were reassessed in LPS-injured cells. Expression level of IRAK1 was examined in miR-206 mimic/inhibitor transfected cells by using RT-qPCR. The effect of IRAK1 on LPS-induced inflammation injury was investigated in MRC-5 cells after transfection with pc-IRAK1 and sh-IRAK1. The effects of miR-206 and IRAK1 on MEK/ERK and JNK pathways were determined by western blot assay. RESULTS: LPS significantly triggered inflammation injury in MRC-5 cells by inhibiting cell viability, suppressing the healing of scratches, inducing cell apoptosis, down-regulating Bcl-2 expression and up-regulating Bax, cleaved-Caspase-3 and cleaved-Caspase-9 expression, and concurrently increasing the concentrations and the protein levels of IL-6 and IL-8. MiR-206 overexpression aggravated LPS-induced inflammation injury in MRC-5 cells. Up-regulation of IRAK1 was observed in miR-206 mimic-transfected cells. Moreover, IRAK1 overexpression promoted LPS-induced inflammation injury in MRC-5 cells. MiR-206 activated MEK/ERK and JNK pathways by regulating IRAK1. CONCLUSIONS: MiR-206 promotes LPS-induced inflammation injury through regulation of IRAK1 in MRC-5 cells.