Combining antibiotics with propolis is an effective method to combat bacterial drug resistance. Nanoparticles are of interest in the antimicrobial field because of their higher drug stability, solubility, penetration power, and treatment efficacy. In this study, propolis nanoparticles (PNPs) were synthesized, and their antibacterial and anti-biofilm activities against methicillin-resistant Staphylococcus aureus (MRSA) in combination with ampicillin sodium (AS) were analyzed. The PNPs had an average particle diameter of 118.0 nm, a polydispersity index of 0.129, and a zeta potential of −28.2 mV. The fractional inhibitory concentration indices of PNPs and AS against tested MRSA strains highlighted this synergy, ranging between 0.375 and 0.5. Crystal violet staining showed that combined PNPs and AS significantly inhibited biofilm formation and reduced existing biofilm biomass. We then discovered that PNPs inhibited bacterial adhesion, extracellular polysaccharide synthesis, and mecR1, mecA, blaZ, and icaADBC gene expression. These results indicated that PNPs exerted a synergistic antibacterial effect with AS by inhibiting mecR1, mecA, and blaZ gene expressions to reduce the drug resistance of MRSA. Meanwhile, PNPs weakened bacterial adhesion and aggregation by suppressing icaADBC gene expression, allowing antibiotics to penetrate the biofilm, and exhibiting significant synergistic anti-biofilm activity. In summary, PNPs are promising candidates for combating MRSA-related diseases.
Ursodeoxycholic acid (UDCA) can be used as a drug to treat various liver and bile diseases. Currently, the biological synthesis of UDCA is predominantly conducted via a two-step enzymatic process in which synthesis is catalyzed by 7α-hydroxysteroid dehydrogenase (7α-HSDH) and 7β-hydroxysteroid dehydrogenase (7β-HSDH) in succession, utilizing chenodeoxycholic acid (CDCA) as the substrate. In this study, an engineered Escherichia coli (E. coli) strain, designated UCA23, was constructed. This strain coexpressed four enzymes under the control of three independent T7 promoters: lactate dehydrogenase (LDH) derived from Lactobacillus delbrueckii, glucose dehydrogenase (GDH) derived from Priestia megaterium, 7α-HSDH derived from E. coli, and 7β-HSDH derived from Ruminococcus torques, enabling the whole-cell catalytic synthesis of UDCA from CDCA. This study systematically optimized the reaction parameters, including temperature, pH, and the addition of organic solvents and surfactants, for the whole-cell catalytic synthesis of UDCA by UCA23, and at the 2 L level, a UDCA conversion rate of 99% was achieved with 100 mM CDCA in 2 h, which is the highest level of conversion of a high-concentration CDCA substrate reported to date.
Eutrophication facilitates the proliferation of cyanobacteria, ultimately leading to the formation of harmful cyanobacterial blooms. Prodigiosin, known for its algicidal properties, presents significant potential for application in water pollution remediation. This study aims to identify and characterize a novel strain with superior prodigiosin production capabilities and to elucidate the algicidal mechanism of prodigiosin against Microcystis aeruginosa and Anabaena sp. by assessing the photosynthetic responses of algal cells in the presence of prodigiosin. The findings revealed the isolation and identification of a new strain, ZC52, classified as Serratia marcescens. The optimal medium composition was determined to be 20.0 mL·L−1 glycerol, 15.0 g·L−1 beef bone peptone, 15.0 g·L−1 magnesium sulfate heptahydrate, 0.15 g·L−1 corn dry powder, and 0.250% tyrosine, resulting in a 47.40% increase in prodigiosin yield, thereby achieving a production level of 7.644 g·L−1. Moreover, the algicidal activity exhibited a concentration-dependent relationship, with 10.0 mg·L−1 of prodigiosin leading to approximately 53.25% and 30.44% inhibition of chlorophyll a content within 24 h, demonstrating the potential of prodigiosin as an effective algicidal compound. Meanwhile, exposure to 10.0 mg·L−1 of prodigiosin resulted in reductions of 46.88% and 21.02% in the Fv/Fm values of M. aeruginosa and Anabaena sp., respectively. Our results indicated that prodigiosin can inhibit the accumulation of photosynthetic pigments and significantly diminish algal photosynthetic efficiency. This study not only identifies valuable microbial resources for prodigiosin production but also provides a theoretical framework and empirical evidence to support the scientific management of cyanobacterial blooms.
Methicillin-resistant Staphylococcus aureus (MRSA) poses a serious threat to public health and can form biofilms to enhance its drug resistance. Caffeic acid phenethyl ester (CAPE), which is primarily extracted from propolis, possesses diverse biological activities. However, its effect on anti-MRSA biofilms and the relevant mechanisms have not been fully clarified. Therefore, this study explored the ability of CAPE to combat MRSA biofilms. The results showed that CAPE has significant antibiofilm activities against MRSA. The minimum inhibitory concentration (MIC) values of CAPE were 256 µg/mL for the MRSA strains ATCC 33591, CI2, and CI3. Crystal violet (CV) assay and XTT assays demonstrated that CAPE could inhibit the formation and consolidation of MRSA CI2 biofilms. Experiments on scanning electron microscopy (SEM), bacterial adhesion assays, and the levels of extracellular polysaccharides confirmed that CAPE can inhibit bacterial adhesion, as well as the synthesis of extracellular polysaccharides in MRSA CI2. Real-time quantitative PCR (RT-qPCR) experiments confirmed that CAPE can affect the expression of MRSA icaADBC, sarA, fnbAB, and clfAB genes. Therefore, the proposed antibiofilm mechanism of CAPE involves the downregulation of aforementioned genes, leading to reduced production of extracellular polysaccharides and adhesion-related proteins, thereby weakening MRSA adhesion and ultimately exerting an antibiofilm effect. In conclusion, these findings suggest CAPE is a promising candidate drug as an antimicrobial agent for managing and preventing biofilm-associated infections caused by MRSA.