Fluorocarbon Plasma-Polymerized Layer Increases the Release Time of Silver Ions and the Antibacterial Activity of Silver-Based Coatings.

Silver-based antibacterial coatings limit the spread of hospital-acquired infections. Indeed, the use of silver and silver oxide nanoparticles (Ag and AgO NPs) incorporated in amorphous hydrogenated carbon (a-C:H) as a matrix demonstrates a promising approach to reduce microbial contamination on environmental surfaces. However, its success as an antibacterial coating hinges on the control of Ag+ release. In this sense, if a continuous release is required, an additional barrier is needed to extend the release time of Ag+. Thus, this research investigated the use of a plasma fluoropolymer (CFx) as an additional top layer to elongate Ag+ release and increase the antibacterial activity due to its high hydrophobic nature. Herein, a porous CFx film was deposited on a-C:H containing Ag and AgO NPs using pulsed afterglow low pressure plasma polymerization. The chemical composition, surface wettability and morphology, release profile, and antibacterial activity were analyzed. Overall, the combination of a-C:H:Ag (12.1 at. % of Ag) and CFx film (120.0°, F/C = 0.8) successfully inactivated 88% of E. coli and delayed biofilm formation after 12 h. Thus, using a hybrid approach composed of Ag NPs and a hydrophobic polymeric layer, it was possible to increase the overall antibacterial activity of the coating.

Porphyromonas gingivalis under palmitate-induced obesogenic microenvironment modulates the inflammatory transcriptional signature of macrophage-like cells.

Metabolic diseases and low-grade chronic inflammation are interconnected: obese persons are at higher risk of developing periodontitis. However, the molecular mechanisms involved in the development and progression of periodontitis in an obesogenic microenvironment in response to periodontopathogens are still lacking. This study aims to investigate the combined effects of palmitate and Porphyromonas gingivalis on the secretion of pro-inflammatory cytokines and on transcriptional landscape modifications in macrophage-like cells. U937 macrophage-like cells were treated with palmitate and stimulated with P. gingivalis for 24h. Cytokines IL-1ß, TNF-α and IL-6 were measured by ELISA in the culture medium and cell extracted RNA was submitted to a microarray analysis followed by Gene Ontology analyses. P. gingivalis, in presence of palmitate, potentiated IL-1ß and TNF-α secretion in comparison to palmitate alone. Gene Ontology analyses also revealed that the combination palmitate-P. gingivalis potentiated the number of gene molecular functions implicated in the regulation of immune and inflammatory pathways compared to macrophages treated with palmitate alone. Our results provide the first comprehensive mapping of gene interconnections between palmitate and P. gingivalis during inflammatory responses in macrophage-like cells. These data highlight the importance of considering systemic conditions, specifically obesogenic microenvironment, in the management of periodontal disease in obese patients.

Multi-Omics Data Integration Reveals Key Variables Contributing to Subgingival Microbiome Dysbiosis-Induced Inflammatory Response in a Hyperglycemic Microenvironment.

Subgingival microbiome dysbiosis promotes the development of periodontitis, an irreversible chronic inflammatory disease associated with metabolic diseases. However, studies regarding the effects of a hyperglycemic microenvironment on host-microbiome interactions and host inflammatory response during periodontitis are still scarce. Here, we investigated the impacts of a hyperglycemic microenvironment on the inflammatory response and transcriptome of a gingival coculture model stimulated with dysbiotic subgingival microbiomes. HGF-1 cells overlaid with U937 macrophage-like cells were stimulated with subgingival microbiomes collected from four healthy donors and four patients with periodontitis. Pro-inflammatory cytokines and matrix metalloproteinases were measured while the coculture RNA was submitted to a microarray analysis. Subgingival microbiomes were submitted to 16s rRNA gene sequencing. Data were analyzed using an advanced multi-omics bioinformatic data integration model. Our results show that the genes krt76, krt27, pnma5, mansc4, rab41, thoc6, tm6sf2, and znf506 as well as the pro-inflammatory cytokines IL-1ß, GM-CSF, FGF2, IL-10, the metalloproteinases MMP3 and MMP8, and bacteria from the ASV 105, ASV 211, ASV 299, Prevotella, Campylobacter and Fretibacterium genera are key intercorrelated variables contributing to periodontitis-induced inflammatory response in a hyperglycemic microenvironment. In conclusion, our multi-omics integration analysis unveiled the complex interrelationships involved in the regulation of periodontal inflammation in response to a hyperglycemic microenvironment.