[30] Bacterial survival in biofilms: Probes for exopolysaccharide and its hydrolysis, and measurements of intra- and interphase mass fluxes

Weiner, Ronald M.; Seagren, Eric A.; Arnosti, Carol; Quintero, Ernesto J.

doi:10.1016/s0076-6879(99)10032-6

Cited by 23 publications

(24 citation statements)

References 64 publications

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“…It was also noted that the pigmentation phenotype correlated with cohesive colonies that came off the agar surface in densely packed masses and with pellicle formation on the surface of glass culture vessels (Jackson and Burrows 1956;Surgalla and Beesley 1969). In retrospect, these findings were the first evidence of Yersinia biofilm formation-pellicle growth and Congo red binding to a polysaccharide ECM are now recognized as typical traits of many bacterial biofilms (Heilmann and Götz 1998;Weiner et al 1999). Perry et al (1990) identified a Y. pestis chromosomal region required for pigmentation, termed the hemin storage (hms) locus; and a four-gene operon in this locus, hmsHFRS, was later implicated (Lillard et al 1997;Pendrak and Perry 1993) (Table 1).…”

Section: The Y Pestis Pigmentation Phenotype Hms Locus and Biofilmmentioning

confidence: 84%

Yersinia pestis Biofilm in the Flea Vector and Its Role in the Transmission of Plague

Hinnebusch¹,

Erickson²

2008

Current Topics in Microbiology and Immunology

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Transmission by fleabite is a relatively recent evolutionary adaptation of Yersinia pestis, the bacterial agent of bubonic plague. To produce a transmissible infection, Y. pestis grows as an attached biofilm in the foregut of the flea vector. Biofilm formation both in the flea foregut and in vitro is dependent on an extracellular matrix (ECM) synthesized by the Yersinia hms gene products. The hms genes are similar to the pga and ica genes of Escherichia coli and Staphylococcus epidermidis, respectively, that act to synthesize a poly-β-1,6-N-acetyl-dglucosamine ECM required for biofilm formation. As with extracellular polysaccharide production in many other bacteria, synthesis of the Hms-dependent ECM is controlled by intracellular levels of cyclic-di-GMP. Yersinia pseudotuberculosis, the food-and water-borne enteric pathogen from which Y. pestis evolved recently, possesses identical hms genes and can form biofilm in vitro but not in the flea. The genetic changes in Y. pestis that resulted in adapting biofilm-forming capability to the flea gut environment, a critical step in the evolution of vector-borne transmission, have yet to be identified. During a flea bite, Y. pestis is regurgitated into the dermis in a unique biofilm phenotype, and this has implications for the initial interaction with the mammalian innate immune response.

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Section: The Y Pestis Pigmentation Phenotype Hms Locus and Biofilmmentioning

confidence: 84%

Yersinia pestis Biofilm in the Flea Vector and Its Role in the Transmission of Plague

Hinnebusch¹,

Erickson²

2008

Current Topics in Microbiology and Immunology

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“…The lungs were fixed in formalin buffer (4% formaldehyde [pH 7.0]; Bie & Berntsen, Copenhagen, Denmark) for at least 1 week, followed by embedding in paraffin wax, and then cut into 5-m sections (26). Mounted sections were stained with hematoxylin and eosin (HE) combined with Alcian blueperiodic acid-Schiff stain for exopolysaccharides (69). The cellular changes were assigned to acute or chronic inflammation groups by a scoring system (27) based on the proportion of PMN and mononuclear leukocytes (MN) in the inflammatory foci.…”

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confidence: 99%

Novel Mouse Model of ChronicPseudomonas aeruginosaLung Infection Mimicking Cystic Fibrosis

et al. 2005

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Pseudomonas aeruginosa causes a chronic infection in the lungs of cystic fibrosis (CF) patients by establishing an alginate-containing biofilm. The infection has been studied in several animal models; however, most of the models required artificial embedding of the bacteria. We present here a new pulmonary mouse model without artificial embedding. The model is based on a stable mucoid CF sputum isolate (NH57388A) with hyperproduction of alginate due to a deletion in mucA and functional N-acylhomoserine lactone (AHL)-based quorumsensing systems. Chronic lung infection could be established in both CF mice (Cftr tmlUnc؊/؊ ) and BALB/c mice, as reflected by the detection of a high number of P. aeruginosa organisms in the lung homogenates at 7 days postinfection and alginate biofilms, surrounded by polymorphonuclear leukocytes in the alveoli. In comparison, both an AHL-producing nonmucoid revertant (NH57388C) from the mucoid isolate (NH57388A) and a nonmucoid isolate (NH57388B) deficient in AHL were almost cleared from the lungs of the mice. This model, in which P. aeruginosa is protected against the defense system of the lung by alginate, is similar to the clinical situation. Therefore, the mouse model provides an improved method for evaluating the interaction between mucoid P. aeruginosa, the host, and antibacterial therapy.

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“…EPS can be analyzed separately from attachment using a dye, CR, that binds to carbohydrates in basic or neutral EPS (68). CR binding is a feature of the hms-dependent biofilm of Y. pestis that occurs during growth at temperatures of up to 34°C (26,28,60).…”

Section: ϫ102mentioning

confidence: 99%

Polyamines Are Essential for the Formation of Plague Biofilm

Patel¹,

Wortham²,

et al. 2006

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We provide the first evidence for a link between polyamines and biofilm levels in Yersinia pestis, the causative agent of plague. Polyamine-deficient mutants of Y. pestis were generated with a single deletion in speA or speC and a double deletion mutant. The genes speA and speC code for the biosynthetic enzymes arginine decarboxylase and ornithine decarboxylase, respectively. The level of the polyamine putrescine compared to the parental speA ؉ speC ؉ strain (KIM6؉) was depleted progressively, with the highest levels found in the Y. pestis ⌬speC mutant (55% reduction), followed by the ⌬speA mutant (95% reduction) and the ⌬speA ⌬speC mutant (>99% reduction). Spermidine, on the other hand, remained constant in the single mutants but was undetected in the double mutant. The growth rates of mutants with single deletions were not altered, while the ⌬speA ⌬speC mutant grew at 65% of the exponential growth rate of the speA ؉ speC ؉ strain. Biofilm levels were assayed by three independent measures: Congo red binding, crystal violet staining, and confocal laser scanning microscopy. The level of biofilm correlated to the level of putrescine as measured by high-performance liquid chromatography-mass spectrometry and as observed in a chemical complementation curve. Complementation of the ⌬speA ⌬speC mutant with speA showed nearly full recovery of biofilm to levels observed in the speA ؉ speC ؉ strain. Chemical complementation of the double mutant and recovery of the biofilm defect were only observed with the polyamine putrescine.

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[30] Bacterial survival in biofilms: Probes for exopolysaccharide and its hydrolysis, and measurements of intra- and interphase mass fluxes

Cited by 23 publications

References 64 publications

Yersinia pestis Biofilm in the Flea Vector and Its Role in the Transmission of Plague

Yersinia pestis Biofilm in the Flea Vector and Its Role in the Transmission of Plague

Novel Mouse Model of ChronicPseudomonas aeruginosaLung Infection Mimicking Cystic Fibrosis

Polyamines Are Essential for the Formation of Plague Biofilm

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