The continuous use of silver nanoparticles (AgNPs) induces drug-resistance in pathogenic bacteria, resulting in the recurrence of biofilms, making them difficult to eradicate. AgNPs in higher concentrations are also toxic to cells. Therefore, an approach that can modulate bacterial quorum sensing (QS) signaling–NP interactions, thereby reducing the production of bacterial pathogenicity traits and minimizing the dose of NPs to suppress bacterial adhesion and colonization, is upmost welcomed. The present work follows an approach where AgNPs are decorated with endolichenic fungus-derived anti-QS chrysophanol (CP-AgNPs) that increases chrysophanol bacterial QS signaling interactions. The advantage of this approach lies in enhancing and long-term preventing bacterial adhesion and subsequent colonization of urinary catheters (UCs) mediated by CP-AgNPs through the inhibition of QS signaling as compared to that with citrate-capped AgNPs (Cc-AgNPs) alone. The anti-adhesion and anti-biofouling effects of CP-AgNPs-coated UC surfaces were assessed for the growth of Pseudomonas aeruginosa PAO1 and Escherichia coli under both static and flow conditions. The CP-AgNPs-coated latex and silicone surfaces showed greater than 9-fold anti-adhesion and anti-biofouling effects than the Cc-AgNPs-coated UCs, which shows the practical applicability of this strategy. These effects of CP-AgNPs influenced the surface hydrophobicity, eDNA content, lipopolysaccharide (LPS) production, and virulence gene expression of bacterial biofilm cells, which reduced biofilm invasion and formation. The CP-AgNPs-coated UCs did not induce toxicity in human bladder fibroblast cells, indicating massive biocompatibility. Eventually, the CP-AgNPs system was successfully applied to prevent bacterial biofilm formation in vivo. Thus, the CP-AgNPs reveal their strong use as anti-adhesion and anti-biofouling coating materials, demonstrating their great potential to prevent UC-associated urinary tract infections.
Both turmeric (Curcuma longa Linn) and honey have been popularly used for treating microbial 28 infections in the Asian countries, but their combined effect on bacterial virulence is not attempted so far. 29 Therefore, in the investigation, the potential of curcumin (50 µg/mL) plus 1% of honey (ChC) in 30 reducing QS-mediated production of virulence factors and biofilm formation in Pseudomonas aeruginosa 31 PAO1 was studied. Treatment of ChC displayed significant reduction in the secretion of AHLs, 32 pyocyanin, pyoverdin, phyochelin, LasA protease, LasB elastase, and hemolysin without affecting 33 bacterium growth. The data obtained from β-galactosidase activity revealed that ChC reduced the activity 34 of QS-related genes namely lasI, lasR, rhlI, and rhlR. The ChC showed strong anti-biofilm activity, 35inhibiting biofilm formation and also eradicating it. It is also proved that anti-biofilm activity is 36 associated with the inhibition of rhamnolipid, alginate, swimming, and swarming motility by ChC. 37Eventually, it was also documented that ChC enhanced the susceptibility of PAO1 to conventional 38 antibiotics. The results clearly indicated that the combination of curcumin and honey is a good candidate 39 for the development of new antibacterial agent acting not as cidal but as anti-virulence agent.
Osteoblast differentiation is critically reduced in various bone-related pathogenesis, including arthritis and osteoporosis. For future development of effective regenerative therapeutics, herein, we reveal the involved molecular mechanisms of a phytoestrogen, ferutinin-induced initiation of osteoblast differentiation from dental pulp-derived stem cell (DPSC). We demonstrate the significantly increased expression level of a transcription factor, Kruppel-like factor 2 (KLF2) along with autophagy-related molecules in DPSCs after induction with ferutinin. The loss-of-function and the gain-of-function approaches of KLF2 confirmed that the ferutinin-induced KLF2 modulated autophagic and OB differentiation-related molecules. Further, knockdown of the autophagic molecule (ATG7 or BECN1) from DPSC resulted not only in a decreased level of KLF2 but also in the reduced levels of OB differentiation-related molecules. Moreover, mitochondrial membrane potential-related molecules were increased and induction of mitophagy was observed in DPSCs after the addition of ferutinin. The reduction of mitochondrial as well as total ROS generations; and induction of intracellular Ca2+ production were also observed in ferutinin-treated DPSCs. To test the mitochondrial respiration in DPSCs, we found that the cells treated with ferutinin showed a reduced extracellular acidification rate (ECAR) than that of their vehicle-treated counterparts. Furthermore, mechanistically, chromatin immunoprecipitation (ChIP) analysis revealed that the addition of ferutinin in DPSCs not only induced the level of KLF2, but also induced the transcriptionally active epigenetic marks (H3K27Ac and H3K4me3) on the promoter region of the autophagic molecule ATG7. These results provide strong evidence that ferutinin stimulates OB differentiation via induction of KLF2-mediated autophagy/mitophagy.
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