Evaluation of alginate-encapsulated Azotobacter chroococcum as a phage-resistant and an effective inoculum

Hammad, A.M.M.

doi:10.1002/(sici)1521-4028(199803)38:1<9::aid-jobm9>3.3.co;2-w

Cited by 8 publications

(10 citation statements)

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“…In vitro biofilm studies have shown that bacterial exopolysaccharides can, in some but not all cases, provide protection against phage (22–24); thus, we next examined whether P. aeruginosa exopolysaccharides protected aggregates from phage-mediated killing. P. aeruginosa PAO1 has the capacity to produce at least three extracellular polysaccharides; alginate, Pel, and Psl.…”

Section: Resultsmentioning

confidence: 99%

“…The reduction in exopolysaccharide mutant biomass after treatment with phage indicates that the mechanism of aggregate tolerance is, at least in part, due to exopolysaccharide production. Exopolysaccharides have been shown to be important for phage tolerance in some, but not all, bacteria (22–24), although these studies have not focused on aggregates. Another possibility is that the presence of Pel and Psl impacts the accessibility or level of the phage receptor.…”

Section: Discussionmentioning

confidence: 99%

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Phage Inhibit Pathogen Dissemination by Targeting Bacterial Migrants in a Chronic Infection Model

Darch

Kragh

Abbott

et al. 2017

mBio

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The microbial communities inhabiting chronic infections are often composed of spatially organized micrometer-sized, highly dense aggregates. It has recently been hypothesized that aggregates are responsible for the high tolerance of chronic infections to host immune functions and antimicrobial therapies. Little is currently known regarding the mechanisms controlling aggregate formation and antimicrobial tolerance primarily because of the lack of robust, biologically relevant experimental systems that promote natural aggregate formation. Here, we developed an in vitro model based on chronic Pseudomonas aeruginosa infection of the cystic fibrosis (CF) lung. This model utilizes a synthetic sputum medium that readily promotes the formation of P. aeruginosa aggregates with sizes similar to those observed in human CF lung tissue. Using high-resolution imaging, we exploited this model to elucidate the life history of P. aeruginosa and the mechanisms that this bacterium utilizes to tolerate antimicrobials, specifically, bacteriophage. In the early stages of growth in synthetic sputum, planktonic cells form aggregates that increase in size over time by expansion. In later growth, migrant cells disperse from aggregates and colonize new areas, seeding new aggregates. When added simultaneously with phage, P. aeruginosa was readily killed and aggregates were unable to form. When added after initial aggregate formation, phage were unable to eliminate all of the aggregates because of exopolysaccharide production; however, seeding of new aggregates by dispersed migrants was inhibited. We propose a model in which aggregates provide a mechanism that allows P. aeruginosa to tolerate phage therapy during chronic infection without the need for genetic mutation.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Phage Inhibit Pathogen Dissemination by Targeting Bacterial Migrants in a Chronic Infection Model

Darch

Kragh

Abbott

et al. 2017

mBio

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“…However, given that the cross-resistance observed was not as strong as the specific resistance evolved, the phages must be binding to the receptors in slightly different ways. Alternatively, phage-mediated selection might have led to both a general resistance mechanism (such as alginate production [37]) that confers resistance to allopatric phages and a more specific resistance (such as restriction modification or CRISPRrelated interference [34]) that confers resistance to the sympatric phage. The fact that we only observed fitness costs associated with resistance in multiple-phage environments is consistent with the accumulation of multiple costly resistance mutations, each conferring specific resistance to sympatric phages.…”

Section: Discussionmentioning

confidence: 99%

The costs of evolving resistance in heterogeneous parasite environments

et al. 2011

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The evolution of host resistance to parasites, shaped by associated fitness costs, is crucial for epidemiology and maintenance of genetic diversity. Selection imposed by multiple parasites could be a particularly strong constraint, as hosts either accumulate costs of multiple specific resistances or evolve a more costly general resistance mechanism. We used experimental evolution to test how parasite heterogeneity influences the evolution of host resistance. We show that bacterial host populations evolved specific resistance to local bacteriophage parasites, regardless of whether they were in single or multiple-phage environments, and that hosts evolving with multiple phages were no more resistant to novel phages than those evolving with single phages. However, hosts from multiple-phage environments paid a higher cost, in terms of population growth in the absence of phage, for their evolved specific resistances than those from single-phage environments. Given that in nature host populations face selection pressures from multiple parasite strains and species, our results suggest that costs may be even more critical in shaping the evolution of resistance than previously thought. Furthermore, our results highlight that a better understanding of resistance costs under combined control strategies could lead to a more 'evolution-resistant' treatment of disease.

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“…), production of extracellular compounds that can prevent phage access to host cells (Doolittle et al. ; Hammad ; Scanlan and Buckling ), or acquisition of novel CRISPR spacers targeting previously encountered phages (Barrangou et al. ), among other mechanisms (Labrie et al.…”

Section: Study Systemmentioning

confidence: 99%

Phage resistance evolution in vitro is not reflective of in vivo outcome in a plant‐bacteria‐phage system*

Hernandez

Koskella

2019

Evolution

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The evolution of resistance to parasites is fundamentally important to disease ecology, yet we remain unable to predict when and how resistance will evolve. This is largely due to the context‐dependent nature of host‐parasite interactions, as the benefit of resistance will depend on the abiotic and biotic environment. Through experimental evolution of the plant pathogenic bacterium Pseudomonas syringae and two lytic bacteriophages across two different environments (high‐nutrient media and the tomato leaf apoplast), we demonstrate that de novo evolution of resistance is negligible in planta despite high levels of resistance evolution in vitro. We find no evidence supporting the evolution of phage‐selected resistance in planta despite multiple passaging experiments, multiple assays for resistance, and high multiplicities of infection. Additionally, we find that phage‐resistant mutants (evolved in vitro) did not realize a fitness benefit over phage‐sensitive cells when grown in planta in the presence of phage, despite reduced growth of sensitive cells, evidence of phage replication in planta, and a large fitness benefit in the presence of phage observed in vitro. Thus, this context‐dependent benefit of phage resistance led to different evolutionary outcomes across environments. These results underscore the importance of studying the evolution of parasite resistance in ecologically relevant environments.

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Evaluation of alginate-encapsulated Azotobacter chroococcum as a phage-resistant and an effective inoculum

Cited by 8 publications

References 0 publications

Phage Inhibit Pathogen Dissemination by Targeting Bacterial Migrants in a Chronic Infection Model

Phage Inhibit Pathogen Dissemination by Targeting Bacterial Migrants in a Chronic Infection Model

The costs of evolving resistance in heterogeneous parasite environments

Phage resistance evolution in vitro is not reflective of in vivo outcome in a plant‐bacteria‐phage system*

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