scholarly journals Fluidic bacterial diodes rectify magnetotactic cell motility in porous environments

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Nicolas Waisbord ◽  
Amin Dehkharghani ◽  
Jeffrey S. Guasto
Keyword(s):  
Disease Transmission ◽  
Biofilm Formation ◽  
Magnetotactic Bacteria ◽  
Survival Strategies ◽  
Higher Dimension ◽  
Pore Scale ◽  
Vascular Networks ◽  
Langevin Model ◽  
Flow Speeds ◽  
Directed Motility

AbstractDirected motility enables swimming microbes to navigate their environment for resources via chemo-, photo-, and magneto-taxis. However, directed motility competes with fluid flow in porous microbial habitats, affecting biofilm formation and disease transmission. Despite this broad importance, a microscopic understanding of how directed motility impacts the transport of microswimmers in flows through constricted pores remains unknown. Through microfluidic experiments, we show that individual magnetotactic bacteria directed upstream through pores display three distinct regimes, whereby cells swim upstream, become trapped within a pore, or are advected downstream. These transport regimes are reminiscent of the electrical conductivity of a diode and are accurately predicted by a comprehensive Langevin model. The diode-like behavior persists at the pore scale in geometries of higher dimension, where disorder impacts conductivity at the sample scale by extending the trapping regime over a broader range of flow speeds. This work has implications for our understanding of the survival strategies of magnetotactic bacteria in sediments and for developing their use in drug delivery applications in vascular networks.

scholarly journals A Compass To Boost Navigation: Cell Biology of Bacterial Magnetotaxis

2020 ◽  
Vol 202 (21) ◽  
Author(s):  
Frank D. Müller ◽  
Dirk Schüler ◽  
Daniel Pfeiffer
Keyword(s):  
Magnetic Field ◽  
Cell Biology ◽  
Molecular Mechanisms ◽  
Magnetotactic Bacteria ◽  
Genetically Engineered ◽  
Model Organisms ◽  
Complex Cell ◽  
Magnetite Biomineralization ◽  
Directed Motility ◽  
The Impact

ABSTRACT Magnetotactic bacteria are aquatic or sediment-dwelling microorganisms able to take advantage of the Earth’s magnetic field for directed motility. The source of this amazing trait is magnetosomes, unique organelles used to synthesize single nanometer-sized crystals of magnetic iron minerals that are queued up to build an intracellular compass. Most of these microorganisms cannot be cultivated under controlled conditions, much less genetically engineered, with only few exceptions. However, two of the genetically amenable Magnetospirillum species have emerged as tractable model organisms to study magnetosome formation and magnetotaxis. Recently, much has been revealed about the process of magnetosome biogenesis and dedicated structures for magnetosome dynamics and positioning, which suggest an unexpected cellular intricacy of these organisms. In this minireview, we summarize new insights and place the molecular mechanisms of magnetosome formation in the context of the complex cell biology of Magnetospirillum spp. First, we provide an overview on magnetosome vesicle synthesis and magnetite biomineralization, followed by a discussion of the perceptions of dynamic organelle positioning and its biological implications, which highlight that magnetotactic bacteria have evolved sophisticated mechanisms to construct, incorporate, and inherit a unique navigational device. Finally, we discuss the impact of magnetotaxis on motility and its interconnection with chemotaxis, showing that magnetotactic bacteria are outstandingly adapted to lifestyle and habitat.

Evidence of cannibalism during long-term biofilm-antimicrobials interaction

2020 ◽  
Author(s):  
Maria Chiara Sportelli ◽  
Giada Caniglia ◽  
Ruggiero Quarto ◽  
Rosaria Anna Picca ◽  
Antonio Valentini ◽  
...  
Keyword(s):  
Biofilm Formation ◽  
Extracellular Polymeric Substances ◽  
Antimicrobial Agents ◽  
Survival Strategies ◽  
Bacterial Cells ◽  
Ion Release ◽  
Swelling Properties ◽  
Morphological Studies ◽  
Molecular Information

<p>Biofilms are considered a major cause of serious health issues in human medicine and food industry, due to their resistance against harsh conditions and pharmacological treatment [1]. Biofilms are defined as three-dimensional structures encasing bacterial communities rooted in extracellular polymeric substances (EPS). These complex systems are strongly influenced by a variety of parameters including biofilm age, external conditions, nutrient deficiency, attack of exogenous agents [2]. Moreover, bacterial colonies may activate survival strategies when subjected to stress such as the presence of antimicrobial agents. Even cannibalistic behavior may occur [3], which involves the secretion of cannibalism toxins inducing the generation of lysed cells providing nutrients.</p> <p>Several methodologies were developed for or adapted to biofilm formation studies enabling a more comprehensive understanding of biofilm physiology, structure, and composition. This information should facilitate the development of more effective eradication strategies. Infrared spectroscopy in attenuated total reflectance (IR-ATR) mode provides in-situ and close to real time monitoring of biofilm lifecycles providing molecular information on the various stages of biofilm formation. Given the antibiotic resistance of biofilms [4], it is of increasing importance to develop innovative methodologies for the treatment of biofilm-related infections. While our research team has shown the generic utility of antimicrobial nanoparticles (NPs) such as ZnONPs, AgNPs, CuNPs, etc. in the past [5], the current study focuses on AgNPs embedded within fluoropolymer matrices with tunable loading of the NPs. Next to morphological studies by TEM and AFM, detailed XPS investigations revealed the surface chemical composition. In addition, the kinetics of antimicrobial ion release enabled correlating the behavior of the nanocomposite to its swelling properties and 3D modification after immersion in liquids. Biofilm growth and inhibition was studied via AFM, optical microscopy and IR-ATR. The IR analysis of the biofilm allowed collecting molecular information on the biofilm behavior during long-term contact with antimicrobial surfaces. It was demonstrated that bacterial cells may re-colonize on top of dead biomass once the latter is thick enough to prevent direct interaction with the antimicrobial surface. In summary, this study represents an excellent foundation for developing an in depth understanding on the behavior of bacterial colonies and nascent biofilms in contact with surfaces decorated with nanoantimicrobials over extended periods of time. It is anticipated that an improved understanding on the stages of biofilm formation provides insight into the processes governing antimicrobial resistance phenomena. Finally, present antimicrobial material may be a useful strategy against Corona viruses. An outlook to this urging topic will be also presented.</p> <div> <p>[1] N. Billings et al., Rep. Prog. Phys., 2015, 78, 036601. [2] D.O. Serra et al., MBio., 2013, 4, e00103. [3] C. Höfler et al., Microbiology, 2016, 162, 164. [4] M.C. Sportelli et al., Sci. Rep., 2017, 7, 11870. [5] M.C. Sportelli et al., TrAC, 2016, 84, 131.</p> </div>

scholarly journals Cooperative Evolutionary Strategy between the Bacteriome and Mycobiome

mBio ◽  
2016 ◽  
Vol 7 (6) ◽  
Author(s):  
Mahmoud Ghannoum
Keyword(s):  
Biofilm Formation ◽  
Extracellular Enzymes ◽  
Chronic Wounds ◽  
Apoptotic Cell ◽  
Fungal Communities ◽  
Survival Strategies ◽  
Evolutionary Strategy ◽  
Evolutionary Strategies ◽  
Bacterial Biofilms ◽  
Microbial Dysbiosis

ABSTRACTNonhealing chronic wounds are all unique in origin and circumstance, and attempting to isolate a single etiology for the failure of a wound to heal is daunting. Wounds represent complex systems of multispecies fungal and bacterial biofilms. The survival strategies of interactive microbial communities have led to cooperative evolutionary strategies that culminate in biofilm formation. In microbial dysbiosis, biofilms are beneficial to both bacterial and fungal communities but detrimental to the host. Fungi benefit by a surge in their virulence factors, while bacteria become tolerant to antibacterials as a consequence of living under the protective umbrella of the biofilm matrix. This interkingdom cooperation negatively impacts the host, as the fungi and bacteria produce extracellular enzymes that inflict tissue damage, leading to an increase in proinflammatory cytokines, which results in oxidative damage and apoptotic cell death.

scholarly journals Identification of signaling pathways, matrix-digestion enzymes, and motility components controllingVibrio choleraebiofilm dispersal

2020 ◽  
Vol 117 (51) ◽  
pp. 32639-32647
Author(s):  
Andrew A. Bridges ◽  
Chenyi Fei ◽  
Bonnie L. Bassler
Keyword(s):  
Disease Transmission ◽  
Biofilm Formation ◽  
Cell Attachment ◽  
Sensory System ◽  
Signaling Proteins ◽  
Matrix Degradation ◽  
Three Stages ◽  
Matrix Production ◽  
Biofilm Dispersal ◽  
Signal Transduction Proteins

Bacteria alternate between being free-swimming and existing as members of sessile multicellular communities called biofilms. The biofilm lifecycle occurs in three stages: cell attachment, biofilm maturation, and biofilm dispersal.Vibrio choleraebiofilms are hyperinfectious, and biofilm formation and dispersal are considered central to disease transmission. While biofilm formation is well studied, almost nothing is known about biofilm dispersal. Here, we conducted an imaging screen forV. choleraemutants that fail to disperse, revealing three classes of dispersal components: signal transduction proteins, matrix-degradation enzymes, and motility factors. Signaling proteins dominated the screen and among them, we focused on an uncharacterized two-component sensory system that we term DbfS/DbfR for dispersal of biofilm sensor/regulator. Phospho-DbfR represses biofilm dispersal. DbfS dephosphorylates and thereby inactivates DbfR, which permits dispersal. Matrix degradation requires two enzymes: LapG, which cleaves adhesins, and RbmB, which digests matrix polysaccharides. Reorientation in swimming direction, mediated by CheY3, is necessary for cells to escape from the porous biofilm matrix. We suggest that these components act sequentially: signaling launches dispersal by terminating matrix production and triggering matrix digestion, and subsequent cell motility permits escape from biofilms. This study lays the groundwork for interventions aimed at modulatingV. choleraebiofilm dispersal to ameliorate disease.

scholarly journals Effects of Sequential Campylobacter jejuni 81-176 Lipooligosaccharide Core Truncations on Biofilm Formation, Stress Survival, and Pathogenesis

2010 ◽  
Vol 192 (8) ◽  
pp. 2182-2192 ◽  
Author(s):  
Mizue Naito ◽  
Emilisa Frirdich ◽  
Joshua A. Fields ◽  
Mark Pryjma ◽  
Jianjun Li ◽  
...  
Keyword(s):  
Campylobacter Jejuni ◽  
Biofilm Formation ◽  
Cell Envelope ◽  
Polymyxin B ◽  
Outer Core ◽  
Survival Strategies ◽  
Calcofluor White ◽  
Stress Survival ◽  
Insight Into

ABSTRACTCampylobacter jejuniis a highly prevalent human pathogen for which pathogenic and stress survival strategies remain relatively poorly understood. We previously found that aC. jejunistrain 81-176 mutant defective for key virulence and stress survival attributes was also hyper-biofilm and hyperreactive to the UV fluorescent dye calcofluor white (CFW). We hypothesized that screening for CFW hyperreactive mutants would identify additional genes required forC. jejunipathogenesis properties. Surprisingly, two such mutants harbored lesions in lipooligosaccharide (LOS) genes (waaFandlgtF), indicating a complete loss of the LOS outer core region. We utilized this as an opportunity to explore the role of each LOS core-specific moiety in the pathogenesis and stress survival of this strain and thus also constructed ΔgalTand ΔcstIImutants with more minor LOS truncations. Interestingly, we found that mutants lacking the LOS outer core (ΔwaaFand ΔlgtFbut not ΔgalTor ΔcstIImutants) exhibited enhanced biofilm formation. The presence of the complete outer core was also necessary for resistance to complement-mediated killing. In contrast, any LOS truncation, even that of the terminal sialic acid (ΔcstII), resulted in diminished resistance to polymyxin B. The cathelicidin LL-37 was found to be active againstC. jejuni, with the LOS mutants exhibiting modest but tiled alterations in LL-37 sensitivity. The ΔwaaFmutant but not the other LOS mutant strains also exhibited a defect in intraepithelial cell survival, an aspect ofC. jejunipathogenesis that has only recently begun to be clarified. Finally, using a mouse competition model, we now provide the first direct evidence for the importance of theC. jejuniLOS in host colonization. Collectively, this study has uncovered novel roles for theC. jejuniLOS, highlights the dynamic nature of theC. jejunicell envelope, and provides insight into the contribution of specific LOS core moieties to stress survival and pathogenesis.

scholarly journals Biofilms: Formation, Properties, Impact on Industries, Strategies for Control

2013 ◽  
Vol 12 (4) ◽  
pp. 29-54
Author(s):  
Kavitha Panicker Chandan S V
Keyword(s):  
Biofilm Formation ◽  
Food Industry ◽  
Survival Strategies ◽  
Harsh Environments ◽  
Porous Structures ◽  
Paper Manufacturing ◽  
Multicellular Structure ◽  
The Earth ◽  
Industrial Setting ◽  
Wide Range

Microbes being one of the oldest inhabitants on the earth, have successfully survived the harsh environments by a number of survival strategies. One such strategy is the formation of a multicellular structure formed by the adherence of the microorganisms to a surface, known as biofilm. This structure is formed by first reversible and then irreversible linkages with the solid support. These are the porous structures with micro colonies, enclosed by exopolysaccharides and are connected by interstitial voids called water channels to promote the influx of nutrients, oxygen and other vital molecules and the efflux of metabolic wastes. Biofouling – formation of biofilms in an industrial setting has been a major problem in the wide range of industries with deleterious effects. The challenges brought about by biofilms in various sectors of the food industry, paper manufacturing and marine industries as well as other technological problems are discussed. Over the years several strategies are used targeting various stages and site of biofilm formation have been formulated to rid industries of biofilms once and for all. Though there exists no ‘perfect solution’ for complete biofilm eradication to date, some of the more recent and potential strategies will be discussed

scholarly journals Identification and analysis of the signaling pathways, matrix-digestion enzymes, and motility components controlling Vibrio cholerae biofilm dispersal

2020 ◽  
Author(s):  
Andrew Bridges ◽  
Chenyi Fei ◽  
Bonnie Bassler
Keyword(s):  
Vibrio Cholerae ◽  
Disease Transmission ◽  
Biofilm Formation ◽  
Cell Attachment ◽  
Sensory System ◽  
Signaling Proteins ◽  
Matrix Degradation ◽  
Three Stages ◽  
Biofilm Dispersal ◽  
Signal Transduction Proteins

Abstract Bacteria alternate between being free-swimming and existing as members of sessile multicellular communities called biofilms. The biofilm lifecycle occurs in three stages: cell attachment, biofilm maturation, and biofilm dispersal. Vibrio cholerae biofilms are hyper-infectious and biofilm formation and dispersal are considered central to disease transmission. While biofilm formation is well-studied, almost nothing is known about biofilm dispersal. Here, we conduct an imaging screen for V. cholerae mutants that fail to disperse, revealing three classes of dispersal components: signal transduction proteins, matrix-degradation enzymes, and motility factors. Signaling proteins dominated the screen and among them, we focused on an uncharacterized two-component sensory system that we name DbfS/DbfR for Dispersal of Biofilm Sensor/Regulator. Phospho-DbfR represses biofilm dispersal. DbfS dephosphorylates and thereby inactivates DbfR, which permits dispersal. Matrix degradation requires two enzymes: LapG, which cleaves adhesins, and RbmB, which digests matrix polysaccharide. Reorientations in swimming direction, mediated by CheY3, are necessary for cells to escape from the porous biofilm matrix. We suggest that these components act sequentially: signaling launches dispersal by terminating matrix production and triggering matrix digestion and, subsequently, cell motility permits escape from biofilms. This study lays the groundwork for interventions that modulate V. cholerae biofilm dispersal to ameliorate disease.

Driving factors for bioclogging of pores and porous media

2020 ◽  
Author(s):  
Dorothee Kurz ◽  
Eleonora Secchi ◽  
Roman Stocker ◽  
Joaquin Jimenez-Martinez
Keyword(s):  
Porous Medium ◽  
Porous Media ◽  
Biofilm Formation ◽  
Driving Factors ◽  
High Temporal Resolution ◽  
Pore Scale ◽  
Biofilm Growth ◽  
Medium Scale ◽  
Biofilm Development ◽  
Biofilm Structure

<p>Understanding the interplay between hydrodynamics and biogeochemical processes is of growing importance in environmental applications and studies, especially in the fields of bioremediation and ecology. The majority of the microbial communities living in soil have a surface-attached lifestyle, allowing them to form biofilms. The biofilm growth influences pore geometries by clogging them and thus redirecting the flow, which in return affects biofilm development and local mass transport. After initially clogging single pores, the biofilm structure expands to larger clusters before eventually clogging the porous medium entirely. We study these processes with a soil-born microorganism, <em>Bacillus subtilis</em>, in microfluidic devices mimicking porous media to get a mechanistic understanding of the driving factors of bioclogging of porous media on different scales.</p> <p>Carefully designed porous geometries were used for the experiments to study biofilm growth under different flow conditions. After being seeded with bacteria, devices were exposed to a continuous nutrient flow during several days. Continuously monitoring the pressure evaluation and imaging the biofilm growth using Brightfield microscopy allowed a high temporal resolution of biofilm growth processes.</p> <p>An interplay of hydraulic parameters and geometric features of the porous medium as well as the mass flow rate of nutrients drive the speed of pore clogging. Besides the pore scale clogging, the initiation of biofilm formation as well as the speed of clogging of the entire medium are influenced by the before mentioned parameters. Furthermore, the size and number of the biofilm clusters formed seem to drive the medium scale clogging. This leads to inverting trends concerning the clogging rate in one pore when compared to the porous medium scale for different pore sizes. These results shed light on the pore-scale mechanism as well as driving parameters of biofilm formation and bioclogging and their transferability to the next larger scale, e.g. a porous medium.</p>

scholarly journals Motility and Chemotaxis in Agrobacterium tumefaciens Surface Attachment and Biofilm Formation

2007 ◽  
Vol 189 (22) ◽  
pp. 8005-8014 ◽  
Author(s):  
Peter M. Merritt ◽  
Thomas Danhorn ◽  
Clay Fuqua
Keyword(s):  
Agrobacterium Tumefaciens ◽  
Biofilm Formation ◽  
Bacterial Species ◽  
Wild Type ◽  
Swarming Motility ◽  
Surface Attachment ◽  
Directed Motility ◽  
Suppressor Mutants ◽  
Static Conditions ◽  
Specific Deletion

ABSTRACT Bacterial motility mechanisms, including swimming, swarming, and twitching, are known to have important roles in biofilm formation, including colonization and the subsequent expansion into mature structured surface communities. Directed motility requires chemotaxis functions that are conserved among many bacterial species. The biofilm-forming plant pathogen Agrobacterium tumefaciens drives swimming motility by utilizing a small group of flagella localized to a single pole or the subpolar region of the cell. There is no evidence for twitching or swarming motility in A. tumefaciens. Site-specific deletion mutations that resulted in either aflagellate, flagellated but nonmotile, or flagellated but nonchemotactic A. tumefaciens derivatives were examined for biofilm formation under static and flowing conditions. Nonmotile mutants were significantly deficient in biofilm formation under static conditions. Under flowing conditions, however, the aflagellate mutant rapidly formed aberrantly dense, tall biofilms. In contrast, a nonmotile mutant with unpowered flagella was clearly debilitated for biofilm formation relative to the wild type. A nontumbling chemotaxis mutant was only weakly affected with regard to biofilm formation under nonflowing conditions but was notably compromised in flow, generating less adherent biomass than the wild type, with a more dispersed cellular arrangement. Extragenic suppressor mutants of the chemotaxis-impaired, straight-swimming phenotype were readily isolated from motility agar plates. These mutants regained tumbling at a frequency similar to that of the wild type. Despite this phenotype, biofilm formation by the suppressor mutants in static cultures was significantly deficient. Under flowing conditions, a representative suppressor mutant manifested a phenotype similar to yet distinct from that of its nonchemotactic parent.

scholarly journals Identification of signaling pathways, matrix-digestion enzymes, and motility components controlling Vibrio cholerae biofilm dispersal

2020 ◽  
Author(s):  
Andrew A. Bridges ◽  
Chenyi Fei ◽  
Bonnie L. Bassler
Keyword(s):  
Signal Transduction ◽  
Vibrio Cholerae ◽  
Disease Transmission ◽  
Biofilm Formation ◽  
Cell Attachment ◽  
Sensory System ◽  
Matrix Degradation ◽  
Free Swimming ◽  
Molecular Events ◽  
Biofilm Dispersal

AbstractBacteria alternate between being free-swimming and existing as members of sessile multicellular communities called biofilms. The biofilm lifecycle occurs in three stages: cell attachment, biofilm maturation, and biofilm dispersal. Vibrio cholerae biofilms are hyper-infectious and biofilm formation and dispersal are considered central to disease transmission. While biofilm formation is well-studied, almost nothing is known about biofilm dispersal. Here, we conduct an imaging screen for V. cholerae mutants that fail to disperse, revealing three classes of dispersal components: signal transduction proteins, matrix-degradation enzymes, and motility factors. Signaling proteins dominated the screen and among them, we focused on an uncharacterized two-component sensory system that we name DbfS/DbfR for Dispersal of Biofilm Sensor/Regulator. Phospho-DbfR represses biofilm dispersal. DbfS dephosphorylates and thereby inactivates DbfR, which permits dispersal. Matrix degradation requires two enzymes: LapG, which cleaves adhesins, and RbmB, which digests matrix polysaccharide. Reorientations in swimming direction, mediated by CheY3, are necessary for cells to escape from the porous biofilm matrix. We suggest that these components act sequentially: signaling launches dispersal by terminating matrix production and triggering matrix digestion and, subsequently, cell motility permits escape from biofilms. This study lays the groundwork for interventions that modulate V. cholerae biofilm dispersal to ameliorate disease.Significance statementThe pathogen Vibrio cholerae alternates between the free-swimming state and existing in sessile multicellular communities known as biofilms. Transitioning between these lifestyles is key for disease transmission. V. cholerae biofilm formation is well studied, however, almost nothing is known about how V. cholerae cells disperse from biofilms, precluding understanding of a central pathogenicity step. Here, we conducted a high-content imaging screen for V. cholerae mutants that failed to disperse. Our screen revealed three classes of components required for dispersal: signal transduction, matrix degradation, and motility factors. We characterized these components to reveal the sequence of molecular events that choreograph V. cholerae biofilm dispersal. Our report provides a framework for developing strategies to modulate biofilm dispersal to prevent or treat disease.

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