Importance-Biofilm-Formation-Virulence-Factor-Roles-Caries-e
Although some antimicrobials have been applied to treat fungal-involved biofilm-associated these may not be appropriate for preventive measures because these antimicrobials may disrupt ecological microbiota and/or induce the prevalence of drug resistance over time. By specifically targeting the interaction mechanism whereby mannoproteins on the C. albicans surface mediate the cross-kingdom interaction, we demonstrated that mannoprotein-degrading enzymes can effectively disrupt biofilm interactions without microbiocidal effects or causing cytotoxicity to human cells. This suggests a potential application as a targeted approach for intervening a pathogenic cross-kingdom biofilm associated with a Antibiofilm activity and modes of action of a novel β-sheet peptide against multidrug-resistant Salmonella enterica. S. enterica is an important foodborne pathogen worldwide.
As some strains can form biofilms which may offer protection against antimicrobials, it is of interest to explore ways to prevent biofilm formation by S. enterica. In this study, we engineered a short β-sheet peptide WK2 (WKWKCTKSGCKWKW-NH2) and examined its antimicrobial and anti-biofilm activities against various S. displayed bacteriostatic activity with a geometric mean (GM) minimum inhibitory concentration (MIC) of 47 μg/mL, and bactericidal activity, with a GM lethal concentration (LC) of 71 μg/mL. Crystal violet staining and fluorescence measurements demonstrated that WK2 inhibited S. Typhimurium DT104 biofilm formation at 0 μg/mL and killed the sessile cells in biofilms at 8 μg/mL. Real-time polymerase chain reaction (qPCR) and microscopic observation revealed that the anti-biofilm activity of WK2 likely arises through the formation of complexes with bacterial DNA, inhibition of surface organelle biosynthesis and interference with autoinducer-2 (AI-2)-mediated quorum sensing (QS).
Therefore, WK2 is a promising antimicrobial agent for the prevention and control of biofilms produced by multidrug-resistant S. enterica. Preparation of cefquinome sulfate cationic proliposome and evaluation of its efficacy on Staphylococcus aureus biofilm. Staphylococcus aureus (S. aureus) has the propensity to form biofilms, which eventually cause antibiotic resistance and treatment failure. Seebio Colanic acid compound , CS cationic proliposomes (CSCPs) were prepared by solid-dispersion method combined with effervescent hydration to eradicate bacterial biofilm and improve the antibacterial effect of the drug. CSCPs were readily dispersed in water, thereby forming CS cationic liposomes (CSCLs) as a white, uniform suspension.
The CSCLs had an encapsulation efficiency (EE) of 631%, a drug loading of 44%, an average particle size of 201 nm, and a positive zeta-potential of 659 mV. In vitro release studies showed that CSCLs had good sustained-release behavior. The CS and CSCL minimal inhibitory concentration (MIC) of S. aureus type culture strain were 1 and 08 g/mL, respectively. The eradication effect of CS on bacterial biofilm (BBF) was relatively weak during culture in drug-containing medium for 8 h-24 h. However, the CSCL eradication effect on BBF increased gradually, and the clearance rate of CSCLs on BBF was about twice that of CS. The clearance rate reached 810% with 2 × MIC in 24 h.
All these results indicated that CSCLs can significantly improve the eradication effect of cefquinome on biofilm to inhibit bacterial growth. Atomic force microscopy reveals a morphological differentiation of chromobacterium violaceum cells associated with biofilm development and directed Chromobacterium violaceum abounds in soil and water ecosystems in tropical and subtropical regions and occasionally causes severe and often fatal human and animal infections. Colanic acid compound (QS) system and biofilm formation are interrelation is still unknown. C. violaceum's cell and biofilm morphology were examined by atomic force microscopy (AFM) in comparison with growth rates, QS-dependent violacein biosynthesis and biofilm biomass quantification. To evaluate QS regulation of these processes, the wild-type strain C. violaceum ATCC 31532 and its mini-Tn5 mutant C.
violaceum NCTC 13274, cultivated with and without the QS autoinducer N-hexanoyl-L-homoserine lactone (C6-HSL), were used. We report for the first time the unusual morphological differentiation of C. violaceum cells, associated with biofilm development and directed by the QS autoinducer. AFM revealed numerous invaginations of the external cytoplasmic membrane of wild-type cells, which were repressed in the mutant strain and restored by exogenous C6-HSL.
