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Staphylococcus epidermidis is well recognized nosocomial pathogen in clinical settings for their implants associated infections. Biofilm and virulence production executes a S. epidermidis pathogenesis against host. Hence, interfering of biofilm formation has become an auspicious to control the pathogenesis of S. epidermidis. The present study evaluates antibiofilm potential of Rhizophora mucronata against S. epidermidis biofilms. Rhizophora mucronata leaves extract significantly inhibited the biofilm formation and quebrachitol was identified as an active compound responsible for the biofilm inhibition. Quebrachitol significantly inhibited biofilm formation at concentration dependent manner without exhibit non-bactericidal property. And, quebrachitol reduced the biofilm building components such as exopolysaccharides, lipase and proteins production. Confocal laser scanning microscopic studies obtained quebrachitol surface independent biofilm efficacy against S. epidermidis. Notably, quebrachitol significantly reduced S. epidermidis adherence on biotic (coated with type I collagen and fibrinogen) and abiotic (hydrophobic and hydrophilic) surfaces. Addition of quebrachitol inhibits autolysis mediated initial attachment and accumulation associated aggregation process. Moreover, quebrachitol significantly reduced the hydrolases virulence production which supports S. epidermidis invasion into the host. Furthermore, gene expression analysis revealed the ability of quebrachitol to downregulate the virulence genes expression which are mainly involved in biofilm formation and virulence production. The results obtained from the present study suggest that quebrachitol as an ideal candidate for the therapeutic action against S. epidermidis pathogenesis.

Staphylococcus epidermidis is an opportunistic human pathogen, which is involved in numerous nosocomial and implant associated infections. Biofilm formation is one of the prime virulence factors of S. epidermidis that supports its colonization on biotic and abiotic surfaces. The global dissemination of three lineages of S. epidermidis superbugs highlights its clinical significance and the imperative need to combat its pathogenicity. Thus, in the current study, the antibiofilm activity of umbelliferone (UMB), a natural product of the coumarin family, was assessed against methicillin-resistant S. epidermidis (MRSE). UMB exhibited significant antibiofilm activity (83%) at 500 μg/ml concentration without growth alteration. Microscopic analysis corroborated the antibiofilm potential of UMB and unveiled its potential to impair intercellular adhesion, which was reflected in auto-aggregation and solid phase adherence assays. Furthermore, real time PCR analysis revealed the reduced expression of adhesion encoding genes ( icaD, atlE, aap, bhp, ebh, sdrG , and sdrF ). Down regulation of agrA and reduced production of secreted hydrolases upon UMB treatment were speculated to hinder invasive lifestyle of MRSE. Additionally, UMB hindered slime synthesis and biofilm matrix components, which were believed to augment antibiotic susceptibility. In vivo assays using Caenorhabditis elegans divulged the non-toxic nature of UMB and validated the antibiofilm, antivirulence, and antiadherence properties of UMB observed in in vitro assays. Thus, UMB impairs MRSE biofilm by turning down the initial attachment and intercellular adhesion. Altogether, the obtained results suggest the potent antibiofilm activity of UMB and the feasibility of using it in clinical settings for combating S. epidermidis infections., (Copyright © 2019 Swetha, Pooranachithra, Subramenium, Divya, Balamurugan and Pandian.)

Oral bacteria initiate biofilm formation by attaching to tooth surfaces via an interaction of a lectin-like bacterial protein with carbohydrate chains on the pellicle. This study aimed to find naturally derived lectins that inhibit the initial attachment of a cariogenic bacterial species, Streptococcus mutans (S. mutans), to carbohydrate chains in saliva in vitro. Seventy kinds of lectins were screened for candidate motifs that inhibit the attachment of S. mutans ATCC 25175 to a saliva-coated culture plate. The inhibitory effect of the lectins on attachment of the S. mutans to the plates was quantified by crystal violet staining, and the biofilm was observed under a scanning electron microscope (SEM). Surface plasmon resonance (SPR) analysis was performed to examine the binding of S. mutans to carbohydrate chains and the binding of candidate lectins to carbohydrate chains, respectively. Moreover, binding assay between the biotinylated-lectins and the saliva components was conducted to measure the lectin binding. Lectins recognizing a salivary carbohydrate chain, Galβ1-3GalNAc, inhibited the binding of S. mutans to the plate. In particular, Agaricus bisporus agglutinin (ABA) markedly inhibited the binding. This inhibition was confirmed by SEM observation. SPR analysis indicated that S. mutans strongly binds to Galβ1-3GalNAc, and ABA binds to Galβ1-3GalNAc. Finally, the biotinylated Galβ1-3GalNAc-binding lectins including ABA demonstrated marked binding to the saliva components. These results suggest that ABA lectin inhibited the attachment of S. mutans to Galβ1-3GalNAc in saliva and ABA can be useful as a potent inhibitor for initial attachment of oral bacteria and biofilm formation.

Exposure of Salmonella to environmental stress, prior to its adherence to a food contact surface, may change the cell surface properties and consequently affect its initial attachment and biofilm formation. This study investigated the influence of temperature and pH preacclimation on the initial attachment of Salmonella Enteritidis to acrylic and stainless steel. Besides, changes in physicochemical properties of cells were examined; and their surface attachment was modeled by xDLVO theory. Results showed that control cells pre-grown at 37°C had significantly (P<0.05) higher initial attachment, followed by those pre-grown at 25, 42, and 10°C. The initial attachment of cells pre-grown at pH 5.3 or 6.3 was not significantly (P>0.05) different from control cells pre-grown at pH 7.3, but they were significantly higher compared to cells pre-grown at pH 8.3 and 9.0. No significant difference was observed between cell attachment to acrylic and stainless steel, although they had different physicochemical properties. The xDLVO theory successfully explained higher attachment for cells pre-grown at optimal condition on both contact surfaces. However, the xDLVO theory could not explain the similar attachment of cells to acrylic and stainless steel. This study elucidates that commonly used intervention technologies including cold storage, thermal treatment, and alkaline antimicrobial agents might alter the physicochemical properties of S. Enteritidis cells and result in varied initial attachment levels., (Copyright © 2015 Elsevier B.V. All rights reserved.)

Actinomyces naeslundii is an early colonizer with important roles in the development of the oral biofilm. The effects of butyric acid, one of short chain fatty acids in A. naeslundii biofilm formation was observed using a flow cell system with Tryptic soy broth without dextrose and with 0.25% sucrose (TSB sucrose). Significant biofilms were established involving live and dead cells in TSB sucrose with 60mM butyric acid but not in concentrations of 6, 30, 40, and 50mM. Biofilm formation failed in 60mM sodium butyrate but biofilm level in 60mM sodium butyrate (pH4.7) adjusted with hydrochloric acid as 60mM butyric media (pH4.7) was similar to biofilm levels in 60mM butyric acid. Therefore, butyric acid and low pH are required for significant biofilm formation in the flow cell. To determine the mechanism of biofilm formation, we investigated initial A. naeslundii colonization in various conditions and effects of anti-GroEL antibody. The initial colonization was observed in the 60mM butyric acid condition and anti-GroEL antibody inhibited the initial colonization. In conclusion, we established a new biofilm formation model in which butyric acid induces GroEL-dependent initial colonization of A. naeslundii resulting in significant biofilm formation in a flow system., (Copyright © 2014 Elsevier B.V. All rights reserved.)

Human beta-defensin-3 (hBD3) acts as a first line of defense against both Gram-positive and Gram-negative bacteria infection. Streptococci are the significant cause for oral biofilm associated diseases. We synthesized three fragments (hBD3-1, hBD3-2, hBD3-3) from the hBD3 and evaluated the antibacterial efficacy on oral streptococci. All of the three fragments from hBD3 had good estimated solubility and hBD3-3 had a higher net positive charge than others. Structure analysis showed that the three fragments shared stable β-sheet structure, but tyrosine were not found in hBD3-2 and hBD3-3 by using Raman and circular dichroism spectroscopy. The inhibition ability of the peptides was examined on the bioactivity of Streptococcus oralis (S.oralis), Streptococcus sanguinis (S. sanguinis) and Streptococcus gordonii (S. gordonii) by minimal inhibitory concentration, minimum bactericidal concentration and anti-biofilm formation test. Three fragments had antimicrobial activity on planktonic state of streptococci, and S. oralis had much more sensitive to the three peptides. Results of antibiofilm experiment showed that streptococci biofilm formation was more sensitive to hBD3-3. Confocal laser scanning microscopy and scanning electron microscopy showed the decrease of biomass and bacterial morphology destruction, which indicated that the antimicrobial mechanism of hBD3-3 might involve an electrostatic charge-based impact on membrane permeability. In conclusion, hBD3-3 possessed the potential capacity for depressing the growth of bacteria, especially first colonizers during the development of oral biofilm. Powerful, endogenous antimicrobial peptide provides the potential to interfere with biofilm by disorganizing early biofilm formation and thereby inhibiting biofilm-associated diseases. [ABSTRACT FROM AUTHOR]

Biofilm formation is a complex and time-consuming process, especially the attachment and growth of anaerobic biofilm, which fundamentally determines the start-up of biofilm reactor. In this study, biosurfactant, rhamnolipid, was introduced into an anaerobic moving bed biofilm reactor (AnMBBR) to promote its start-up, and the results showed that AnMBBR with rhamnolipid (RMBBR) could be successfully started within 25 days. Compared to the control AnMBBR without rhamnolipid, the start-up time was shortened by about half, the attached biomass on biocarriers was increased to 1.5 times, and the pollutants removal efficiencies were all greatly improved in the start-up phase, especially NO 3 − increased from 86.76 ± 1.04% to 96.93 ± 0.73%, and then these gaps were reduced in the steady-state phase. Under the action of rhamnolipid, the adhesion force of the biofilm increased from 18.9 nN to 27.4 nN eventually, and the interfacial energy between biofilm and biocarriers was transformed from repulsion (6200 KT) to weak attraction (−100 KT) by the evaluation of the extended Derjaguin–Landau–Verwey–Overbeek theory, which significantly promoted the initial attachment of biofilm. The increased metabolic activity, key enzyme activity, extracellular polymeric substances (EPS) and quorum sensing behaviors evidenced that rhamnolipid stimulated microbial internal activities and then regulated biofilm growth process. Moreover, rhamnolipid also significantly enhanced the abundance of functional bacteria in terms of metabolism or quorum sensing, including Thauera , Methylomonas , Desulfomicrobium , Azoarcus , Leptonema. Rhamnolipid would also stimulate the expression of genes that related to membrane transport, biofilm formation and nitrogen metabolism. This work provided a promising strategy for the rapid start-up of anaerobic biofilm reactor. [Display omitted] •Rhamnolipid accelerated the start-up of anaerobic MBBR by promoting biofilm formation. •Multiple regulatory mechanisms of rhamnolipid on biofilm formation were first proposed. •Rhamnolipid changed functional and structural characteristics of cell membrane. •The interfacial energy between biofilm and biocarriers was reduced by rhamnolipid. [ABSTRACT FROM AUTHOR]