Bacterial Swarming:  A Biochemical Time-Resolved FTIR−ATR Study of <i>Proteus mirabilis</i> Swarm-Cell Differentiation

Gué, Michaël; Dupont, Virginie; Dufour, Alain; Sire, Olivier

doi:10.1021/bi010434m

Cited by 50 publications

(29 citation statements)

References 48 publications

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“…Elongated Photorhabdus temperata cells, 50 to 170 m in length were observed in the infected larval hemolymph of the Colorado potato beetle Leptinotarsus decemlineata and are thought to take on this form in response to stress (28). The human urinary tract pathogen Proteus mirabilis also differentiates into large "swarm cells" 20 to 80 m long (29,30), which when grown in vitro, are 10-fold more cytolytic than normal vegetative cells (31). The larger Y. entomophaga cells present at the time when hemocytes are no longer observed may have an alternate function, such as limiting grazing from other organisms, like protozoa.…”

Section: Discussionmentioning

confidence: 99%

Temperature-Dependent Galleria mellonella Mortality as a Result of Yersinia entomophaga Infection

Hurst

Beattie

Jones

et al. 2015

Appl Environ Microbiol

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The bacterium Yersinia entomophaga is pathogenic to a range of insect species, with death typically occurring within 2 to 5 days of ingestion. Per os challenge of larvae of the greater wax moth (Galleria mellonella) confirmed that Y. entomophaga was virulent when fed to larvae held at 25°C but was avirulent when fed to larvae maintained at 37°C. At 25°C, a dose of ϳ4 ؋ 10 7 CFU per larva of a Y. entomophaga toxin complex (Yen-TC) deletion derivative, the Y. entomophaga ⌬TC variant, resulted in 27% mortality. This low level of activity was restored to near-wild-type levels by augmentation of the diet with a sublethal dose of purified Yen-TC. Intrahemocoelic injection of ϳ3 Y. entomophaga or Y. entomophaga ⌬TC cells per larva gave a 4-day median lethal dose, with similar levels of mortality observed at both 25 and 37°C. Following intrahemocoelic injection of a Yen-TC YenA1 green fluorescent protein fusion strain into larvae maintained at 25°C, the bacteria did not fluoresce until the population density reached 2 ؋ 10 7 CFU ml ؊1 of hemolymph. The observed cells also took an irregular form. When the larvae were maintained at 37°C, the cells were small and the observed fluorescence was sporadic and weak, being more consistent at a population density of ϳ3 ؋ 10 9 CFU ml ؊1 of hemolymph. These findings provide further understanding of the pathobiology of Y. entomophaga in insects, showing that the bacterium gains direct access to the hemocoelic cavity, from where it rapidly multiplies to cause disease. The Gram-negative bacterium Yersinia entomophaga was isolated from the cadaver of a Costelytra zealandica (Coleoptera: Scarabaeidae) larva, and has proven consistently pathogenic by per os challenge to this host, as well as to a wide range of coleopteran, lepidopteran, and orthopteran species (1). A 6-day median lethal dose (LD 50 ) was determined as 2.9 ϫ 10 4 Y. entomophaga cells per C. zealandica larva. Following per os challenge with a bacterial dose of ϳ1 ϫ 10 7 Y. entomophaga cells per larva, the larvae typically vomited, expelled frass pellets, changed color from a healthy gray to amber and then a moribund brown, and exhibited reduced feeding activity. By 48 h postingestion, Y. entomophaga cells could be visualized within the hemocoelic cavity of the larvae, after which time death ensued (2).The main virulence determinant of Y. entomophaga is an insect-active toxin complex (TC) derivative termed "Yen-TC" (3). TCs were first identified in the genome of Photorhabdus luminescens (4) and have since been identified in other bacterial genera, including members of the genus Yersinia (5). Typically, TCs are comprised of three proteins, TC-A, TC-B, and TC-C, which combine to form the insect-active complex (6). Yen-TC is comprised of seven subunit proteins: two TC-A-like proteins (YenA1 and YenA2), a TC-B-like protein (YenB), two TC-C-like proteins (YenC1 and YenC2), and two chitinases (Chi1 and Chi2), which combine to form the insect-active TC. Recent structural analysis has revealed that both the Yen-TC and the P. lumine...

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Section: Discussionmentioning

confidence: 99%

Temperature-Dependent Galleria mellonella Mortality as a Result of Yersinia entomophaga Infection

Hurst

Beattie

Jones

et al. 2015

Appl Environ Microbiol

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“…31 Membrane fluidity is higher in P. mirabilis swarm cells compared to their vegetative counterparts, mainly due to the change of lipid composition in the cell membranes (i.e., increase in the content of long and unsaturated fatty acids) after differentiation. 32 As discussed above, 4AP12 interacts with bacterial membrane and may cause cell lysis. The increased fluidity of the cell membrane is likely to retard the formation of stable pores in the phospholipid bilayer, 33 thereby reducing the effect of membrane disruption by 4AP12.…”

Section: Acs Biomaterials Science and Engineeringmentioning

confidence: 96%

Bifunctional Coating with Sustained Release of 4-Amide-piperidine-C12 for Long-Term Prevention of Bacterial Colonization on Silicone

Wang

Chua

Neoh

2015

ACS Biomater. Sci. Eng.

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Bacterial colonization by nosocomial pathogens on medical device surface can cause serious and life-threatening infections. We showed that 4-amide-piperidine-C12 (4AP12), the base form of 4-dodecaneamidepiperidine HCl, has broadspectrum antimicrobial activity against both Gram-negative and Gram-positive bacteria and fungi. Resistance assay confirmed that prolonged exposure of bacteria to subinhibitory concentrations of 4AP12 did not induce resistance to 4AP12. The possible antimicrobial mechanism of 4AP12 was investigated, and attributed to the disruption of the cell membrane of microorganisms and subsequent cell lysis. The hydrophobic 4AP12 was incorporated in Pluronic F127 diacrylate (F127DA) micelles, which were then graft-copolymerized with acrylic acid and cross-linked onto ozonized silicone surface. Sulfobetaine methacrylate and F127DA were then graft-copolymerized as an antifouling layer on top of the F127DA-AA hydrogel containing the 4AP12, thus forming a microscale two-layer bifunctional coating. Sustained release of 4AP12 at a rate of up to 1 μg/day per cm 2 of hydrogel-coated silicone surface was achieved and this was sufficient to inhibit ∼97% of bacterial colonization by Acinetobacter baumannii in artificial urine medium under static condition over a 14-day period. Bacterial colonization by Escherichia coli and Pseudomonas aeruginosa under similar conditions was also significantly reduced. In addition, after 96 h exposure to flowing artificial urine (0.7 mL/min), Escherichia coli colonization on the 4AP12-loaded hydrogel-coated surface was reduced by ∼89% compared to the pristine surface. The concentration of 4AP12 that was released and was effective in inhibiting bacterial colonization did not result in significant cytotoxicity to human epithelial cells.

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“…4). The shift to the swarmer form is accompanied by changes in lipopolysaccharide (LPS), peptidoglycan, and membrane fatty acid composition (59, 60). Swarm cells move together as a group, forming rafts of parallel cells (61).…”

Section: Role Of Flagella In Virulencementioning

confidence: 99%

Proteus mirabilisand Urinary Tract Infections

2015

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Proteus mirabilis is a Gram-negative bacterium which is well-known for its ability to robustly swarm across surfaces in a striking bulls’-eye pattern. Clinically, this organism is most frequently a pathogen of the urinary tract, particularly in patients undergoing long-term catheterization. This review covers P. mirabilis with a focus on urinary tract infections (UTI), including disease models, vaccine development efforts, and clinical perspectives. Flagella-mediated motility, both swimming and swarming, is a central facet of this organism. The regulation of this complex process and its contribution to virulence is discussed, along with the type VI-secretion system-dependent intra-strain competition which occurs during swarming. P. mirabilis uses a diverse set of virulence factors to access and colonize the host urinary tract, including urease and stone formation, fimbriae and other adhesins, iron and zinc acquisition, proteases and toxins, biofilm formation, and regulation of pathogenesis. While significant advances in this field have been made, challenges remain to combatting complicated UTI and deciphering P. mirabilis pathogenesis.

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Bacterial Swarming: A Biochemical Time-Resolved FTIR−ATR Study of Proteus mirabilis Swarm-Cell Differentiation

Cited by 50 publications

References 48 publications

Temperature-Dependent Galleria mellonella Mortality as a Result of Yersinia entomophaga Infection

Temperature-Dependent Galleria mellonella Mortality as a Result of Yersinia entomophaga Infection

Bifunctional Coating with Sustained Release of 4-Amide-piperidine-C12 for Long-Term Prevention of Bacterial Colonization on Silicone

Proteus mirabilisand Urinary Tract Infections

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