Nano-Catechin Gel as a Sustained Release Antimicrobial Agent against Clinically Isolated Porphyromonas gingivalis for Promising Treatment of Periodontal Diseases.

During the last two decades, new drug delivery strategies have been invented that have been able to solve microbial resistance against antibiotics. The goal of the current report was to assess the antimicrobial effects of nano-catechin gels against clinically isolated Porphyromonas gingivalis, one of the main causes of periodontal disease. Catechin-loaded chitosan nanoparticles were prepared by adding a catechin solution to a chitosan solution. Then, the mean particle size and the mean surface charge (zeta potential) of the nanoparticles were detected through photon correlation spectroscopy and zeta sizer, respectively. Nano-catechin gels (1000, 500, 250, 125, 62.5, and 31.2 µg/mL) were prepared, and the antimicrobial assay was performed against clinically isolated Porphyromonas gingivalis (P. gingivalis). The clinically obtained P. gingivalis isolates were obtained from periodontitis patients (N = 15). The consequences are specified as descriptive indices. The normality of data was detected by the Shapiro-Wilk test. Then, to compare the data between groups (with a p value < 0.05 as the significance level), SPSS software (version 22) was used via a Mann-Whitney U test. The results showed a nanometer particle size range and a positive zeta potential for the prepared nanoparticles. All the concentrations (1000, 500, 250, 125, 62.5, and 31.2 µg/mL) of nano-catechin gels showed sustained release patterns and were non-toxic against dental pulp stem cells as well. There were no significant differences between the minimal inhibitory concentrations (MICs) for nano-catechin gel (test group) and Chlorhexidine (control group) against 15 isolates (p > 0.05). Then, two groups showed similar antimicrobial effects. The similar antimicrobial activity of catechin nanoparticles and Chlorhexidine, as a potent antimicrobial agents, against clinically isolated P. gingivalis showed that catechin nanoparticles can be used as a potent antimicrobial material for the treatment of periodontal diseases in the near future.

The role of multiple toll-like receptor signalling cascades on interactions between biomedical polymers and dendritic cells.

Biomaterials are used in several health-related applications ranging from tissue regeneration to antigen-delivery systems. Yet, biomaterials often cause inflammatory reactions suggesting that they profoundly alter the homeostasis of host immune cells such as dendritic cells (DCs). Thus, there is a major need to understand how biomaterials affect the function of these cells. In this study, we have analysed the influence of chemically and physically diverse biomaterials on DCs using several murine knockouts. DCs can sense biomedical polymers through a mechanism, which involves multiple TLR/MyD88-dependent signalling pathways, in particular TLR2, TLR4 and TLR6. TLR-biomaterial interactions induce the expression of activation markers and pro-inflammatory cytokines and are sufficient to confer on DCs the ability to activate antigen-specific T cells. This happens through a direct biomaterial-DC interaction although, for degradable biomaterials, soluble polymer molecules can also alter DC function. Finally, the engagement of TLRs by biomaterials profoundly alters DC adhesive properties. Our findings could be useful for designing structure-function studies aimed at developing more bioinert materials. Moreover, they could also be exploited to generate biomaterials for studying the molecular mechanisms of TLR signalling and DC activation aiming at fine-tuning desired and pre-determined immune responses.

Genotoxic potential of respirable bentonite particles with different quartz contents and chemical modifications in human lung fibroblasts.

Crystalline silica has been classified as a human carcinogen, but there is still considerable controversy regarding its fibrogenic and carcinogenic potential. In the present study, we investigated the genotoxic potential of bentonite particles (diameter < 10 microm) with an a-quartz content of up to 6% and different chemical modifications (alkaline, acidic, organic). Human lung fibroblasts (IMR90) were incubated for 36 h, 48 h, or 72 h with bentonite particles in concentrations ranging from 1 to 15 microg/cm2. Genotoxicity was assessed using the micronucleus (MN) assay and kinetochore analysis. The generation of reactive oxygen species (ROS) caused by bentonite particles via Fenton-like mechanisms was measured acellularly using electron spin resonance (ESR) technique and intracellularly by applying an iron chelator. Our results show that bentonite-induced genotoxic effects in human lung fibroblasts are weak. The formation of micronuclei was only slightly increased after exposure of IMR90 cells to an acidic sample of bentonite dust with a quartz content of 4-5% for 36 h (15 microg/cm2), 48 h (5 microg/cm2), and 72 h (1 microg/cm2), to an alkaline sample with a quartz content of 5% for 48 h and 72 h (15 microg/cm2), and to an acidic bentonite sample with 1% quartz for 72 h (1 microg/cm2). Native (untreated) and organic activated bentonite particles did not show genotoxic effects in most of the experiments. Also, bentonite particles with a quartz content < 1% were negative in the micronucleus assay. Generation of ROS measured by ESR was dependent on the content of transition metals in the sample but not on the quartz content or the chemical modification. Reduction of MN after addition of the iron chelator 2,2'-dipyridyl showed that ROS formation also occurs intracellularly. Altogether, we conclude that the genotoxic potential of bentonite particles is generally low but can be altered by the content of quartz and available transition metals.

ROS-mediated genotoxicity of asbestos-cement in mammalian lung cells in vitro.

Asbestos is a known carcinogen and co-carcinogen. It is a persisting risk in our daily life due to its use in building material as asbestos-cement powder. The present study done on V79-cells (Chinese hamster lung cells) demonstrates the cytotoxic and genotoxic potential of asbestos-cement powder (ACP) in comparison with chrysotile asbestos. A co-exposure of chrysotile and ACP was tested using the cell viability test and the micronucleus assay. The kinetochore analysis had been used to analyse the pathway causing such genotoxic effects. Thiobarbituric acid-reactive substances were determined as evidence for the production of reactive oxygen species. Both, asbestos cement as well as chrysotile formed micronuclei and induced loss of cell viability in a concentration- and time-dependent way. Results of TBARS analysis and iron chelator experiments showed induction of free radicals in ACP- and chrysotile exposed cultures. CaSO4 appeared to be a negligible entity in enhancing the toxic potential of ACP. The co-exposure of both, ACP and chrysotile, showed an additive effect in enhancing the toxicity. The overall study suggests that asbestos-cement is cytotoxic as well as genotoxic in vitro. In comparison to chrysotile the magnitude of the toxicity was less, but co-exposure increased the toxicity of both.