The Consequences of Biofilm Dispersal on the Host

Fleming, Derek; Rumbaugh, Kendra P.

doi:10.1038/s41598-018-29121-2

Cited by 137 publications

(121 citation statements)

References 31 publications

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“…For this, we did not measure biofilm mechanics but rather biofilm dispersal, because we have previously shown that biofilm dispersal in combination with antibiotic therapy is an effective treatment for biofilm infections. 8, 47 Dispersal happens when the bacteria in a biofilm infection convert to the planktonic state; we anticipated that compromising biofilm mechanics would promote dispersal.…”

Section: Resultsmentioning

confidence: 99%

“…Furthermore, we previously found that the generic glycoside hydrolases, which have only minimal effect on biofilms grown in vitro , result in far more dispersal on biofilms grown in the same manner in vivo than do the specific enzymes. 8, 47 One explanation for this apparent discrepancy might be that the changes in biofilms associated with dispersal are not primarily mechanical in nature. Another possibility is that the matrix produced in vivo might not have the same population of polymers as that produced by the same strain in vitro , and therefore might not have appropriately specific targets for the alginate lyase and DNase I.…”

Section: Resultsmentioning

confidence: 99%

“…The glycoside hydrolases cellulase and α–amylase have successfully been used against P. aeruginosa biofilms, disrupting the biofilms and rendering them more susceptible to antibiotics in vivo and in vitro . 8–9 However, these enzymes are not specific against any components of the P. aeruginosa biofilm matrix, and we might expect more specific enzymes to have greater efficiency than generic glycoside hydrolases, with less potential for harming the host. That being said, biofilms formed by different strains of P. aeruginosa are dominated by different types of extracellular polymers (EPS) and will therefore respond differently to enzymes that attack specific polymers.…”

Section: Introductionmentioning

confidence: 99%

“…9 Both cellulase and α-amylase can inhibit P. aeruginosa biofilm growth, and they have been shown to degrade biofilms and render bacteria more susceptible to antibiotics in wounds. 8-9, 36-37…”

Section: Introductionmentioning

confidence: 99%

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Specific Disruption of EstablishedP. aeruginosaBiofilms Using Polymer-Attacking Enzymes

Kovach

Fleming

Rumbaugh

et al. 2019

Preprint

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12Biofilms are communities of bacteria embedded in an extracellular matrix of self-13 produced polymeric substances. This polymer matrix lends the bacteria protection against 14 a wide array of chemical and mechanical stresses that they may experience in their 15 environment, which might be a location in the human body in the case of a biofilm 16 infection, or a surface immersed in fluid in an industrial setting. Breaking down the matrix 17 network renders biofilms more susceptible to physical disruption and to treatments. 18 Different species of bacteria, and different strains within the same species, produce 19 different types of matrix polymersthis suggests that targeting specific polymers for 20 disruption may be more effective than non-specific approaches to disrupting biofilm 21 matrices. In this study, we treated Pseudomonas aeruginosa biofilms with enzymes that 22 are specific to different matrix polymers. We used bulk rheology to measure the resulting 23 approaches to eradicating biofilms in environmental or industrial settings may need to be 40 very different from effective treatments of infection. 41 42 and the importance of a specific polymer type varies with biofilm-forming species and 47 strain. For biofilm infections, the matrix protects the inhabitant bacteria chemically by 48 inhibiting the diffusion of antibiotics into the biofilm and by binding to antibacterial 49 chemicals produced by the host immune response. 1-3 Furthermore, the mechanical 50 integrity and structure of the bacterial biofilm conferred by the matrix gives rise to stable 51 microenvironments that contribute to phenotypic antibiotic tolerance. 4-5 Thus, both the 52 chemical and the structural properties of the biofilm matrix contribute to bacterial 53 tolerance of harsh environments. 54Many common interventions in P. aeruginosa infections, like antibiotic treatment, 55 are far more successful if the bacteria are in a planktonic state rather than in a biofilm. 6

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Specific Disruption of EstablishedP. aeruginosaBiofilms Using Polymer-Attacking Enzymes

Kovach

Fleming

Rumbaugh

et al. 2019

Preprint

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“…Lastly, biofilms enhance the ability of bacteria to generate "persister" sub-populations, which are multi-drug tolerant, essentially dormant cells with a characteristic gene expression signature 24 . Dispersal of a biofilm has the potential to seed a patient with drug-resistant bacteria 25,26 . Strategies are needed to break down biofilms associated with indwelling medical devices and chronic infections, in order to render bacteria sensitive to antibiotics and susceptible to immune clearance.…”

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confidence: 99%

Salmonella Typhimurium biofilm disruption by a human antibody that binds a pan-amyloid epitope on curli

et al. 2020

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Bacterial biofilms, especially those associated with implanted medical devices, are difficult to eradicate. Curli amyloid fibers are important components of the biofilms formed by the Enterobacteriaceae family. Here, we show that a human monoclonal antibody with panamyloid-binding activity (mAb 3H3) can disrupt biofilms formed by Salmonella enterica serovar Typhimurium in vitro and in vivo. The antibody disrupts the biofilm structure, enhancing biofilm eradication by antibiotics and immune cells. In mice, 3H3 injections allow antibioticmediated clearance of catheter-associated S. Typhimurium biofilms. Thus, monoclonal antibodies that bind a pan-amyloid epitope have potential to prevent or eradicate bacterial biofilms.

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