Differential inactivation of glucose- and glutamate dependent acid resistance of Escherichia coli TMW 2.497 by high-pressure treatments

Kilimann, K.V.; Hartmann, C.; Vogel, Rudi F.; Gänzle, Michael G.

doi:10.1016/j.syapm.2005.05.004

Cited by 14 publications

(9 citation statements)

References 32 publications

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“…Treatment of lactic acid bacteria with sublethal pressure is known to inactivate the F 0 F 1 ATPase, as well as ATP-dependent and PMF-dependent MDR transport enzymes, such as LmrP in L. lactis (23). The glutamate-dependent acid resistance system of Escherichia coli is pressure stable (17). The ability to grow in the presence of hops of L. brevis TMW 1.465A and TMW 1.465 was nearly unchanged after inactivation of the membrane-associated transporters.…”

Section: Discussionmentioning

confidence: 99%

Characterization of a Highly Hop-ResistantLactobacillus brevisStrain Lacking Hop Transport

Behr

Gänzle

Vogel

2006

Appl Environ Microbiol

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Resistance to hops is a prerequisite for lactic acid bacteria to spoil beer. In this study we analyzed mechanisms of hop resistance of Lactobacillus brevis at the metabolism, membrane physiology, and cell wall composition levels. The beer-spoiling organism L. brevis TMW 1.465 was adapted to high concentrations of hop compounds and compared to a nonadapted strain. Upon adaptation to hops the metabolism changed to minimize ethanol stress. Fructose was used predominantly as a carbon source by the nonadapted strain but served as an electron acceptor upon adaptation to hops, with concomitant formation of acetate instead of ethanol. Furthermore, hop adaptation resulted in higher levels of lipoteichoic acids (LTA) incorporated into the cell wall and altered composition and fluidity of the cytoplasmic membrane. The putative transport protein HitA and enzymes of the arginine deiminase pathway were overexpressed upon hop adaptation. HorA was not expressed, and the transport of hop compounds from the membrane to the extracellular space did not account for increased resistance to hops upon adaptation. Accordingly, hop resistance is a multifactorial dynamic property, which can develop during adaptation. During hop adaptation, arginine catabolism contributes to energy and generation of the proton motive force until a small fraction of the population has established structural improvements. This acquired hop resistance is energy independent and involves an altered cell wall composition. LTA shields the organism from accompanying stresses and provides a reservoir of divalent cations, which are otherwise scarce as a result of their complexation by hop acids. Some of the mechanisms involved in hop resistance overlap with mechanisms of pH resistance and ethanol tolerance and as a result enable beer spoilage by L. brevis.Resistance to hops is a prerequisite for the ability of lactic acid bacteria to grow in beer and thus cause beer spoilage. Hop compounds, mainly iso-␣-acids, were described as ionophores which dissipate the pH gradient across the cytoplasmic membrane and reduce the proton motive force (PMF). Consequently, the low intracellular pH (pH in ) interferes with essential enzyme reactions and PMF-dependent nutrient uptake is hampered, resulting in the death of cells of hop-sensitive strains (34,37,49).Several mechanisms involved in the hop resistance of lactobacilli have recently been characterized (13, 34-36, 38, 24-44, 47, 48). The proteins contributing to hop resistance include multidrug resistance (MDR) transporters that excrete the hop compounds into the outer medium (35, 45) and proton export systems that maintain the intracellular pH. HitA is a putative divalent cation transporter present predominantly in beerspoiling lactobacilli (13). An alteration of the teichoic acids in the cell wall (50) and a changed lipid composition of the cytoplasmic membranes (34) might additionally contribute to the hop resistance. However, the role of these hop resistance mechanisms in beer-spoiling lactobacilli is not fully understood...

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Section: Discussionmentioning

confidence: 99%

Characterization of a Highly Hop-ResistantLactobacillus brevisStrain Lacking Hop Transport

Behr

Gänzle

Vogel

2006

Appl Environ Microbiol

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“…Escherichia coli TMW2.497 was an E. coli JM109 derivative carrying the gene coding for green fluorescent protein on plasmid pQBI-63 (courtesy of Dr M. Gantzle). 34 Cell Culture and Measurement of In Vitro Permeability T84 human colon cancer epithelial cells were maintained in tissue culture plates (10 cm) in Dulbecco's minimal essential medium/F-12, 10% (vol/vol) heat-inactivated fetal bovine serum, and 1% (wt/vol) penicillin-streptomycin. The cells were plated onto Transwells (2 · 10 5 cells/well, 6.5 mm diameter; 0.4 mm pore size; Corning Life Sciences, Tewksbury, MA) and grown until development of apical junctional complexes (as indicated by a transepithelial electrical resistance [TER] of .2000 V/cm 2 ) for studies.…”

Section: Reagentsmentioning

confidence: 99%

Epithelial Cell Extrusion Leads to Breaches in the Intestinal Epithelium

Liu

Davis²,

Wine

et al. 2013

Inflammatory Bowel Diseases

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“…The in vivo observation of pressure-induced membrane phase transitions was achieved in Lactobacillus plantarum and Lactococcus lactis ( Molina-Gutierrez et al, 2002 ; Ulmer et al, 2002 ) but not in E. coli , where observations of phase transitions of the cytoplasmic membrane are confounded by the outer membrane. The rapid dissipation of the proton motive force by pressure, however, was confirmed in E coli by in situ observation of the pH-dependent GFP fluorescence ( Kilimann et al, 2005 ). Pressure as low as 10 MPa inhibits motility and substrate transport in E. coli ( Bartlett, 2002 ).…”

Section: Pressure Mediated Damage To the Cytoplasmic Membrane Ph Hommentioning

confidence: 99%

“…Remarkably, transport enzymes that are related to pH homeostasis of E. coli exhibit a differential resistance to pressure. Treatment of E. coli with 300 MPa inactivated arginine- and glucose dependent pH homeostasis but not the glutamate decarboxylase system (Figure 2 ; Kilimann et al, 2005 ). Pressure resistance is influenced by membrane fluidity and fatty acid composition ( Casadei et al, 2002 ).…”

Section: Pressure Mediated Damage To the Cytoplasmic Membrane Ph Hommentioning

confidence: 99%

“…The post pressure survival of target organisms is as relevant as the direct lethal effect of pressure treatment. Depending on the choice of food matrix, pH, and target organism, a post-treatment quarantine period allows for the elimination of surviving bacterial cells ( Garcia-Graells et al, 1998 ; Jordan et al, 2001 ; Kilimann et al, 2005 ). However, post-pressure storage or incubation also supports resuscitation of injured cells that were undetectable after pressure treatment ( Garriga et al, 2004 ; Koseki and Yamamoto, 2006 ).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Mechanisms of pressure-mediated cell death and injury in Escherichia coli: from fundamentals to food applications

Gänzle

Liu

2015

Front. Microbiol.

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High hydrostatic pressure is commercially applied to extend the shelf life of foods, and to improve food safety. Current applications operate at ambient temperature and 600 MPa or less. However, bacteria that may resist this pressure level include the pathogens Staphylococcus aureus and strains of Escherichia coli, including shiga-toxin producing E. coli. The resistance of E. coli to pressure is variable between strains and highly dependent on the food matrix. The targeted design of processes for the safe elimination of E. coli thus necessitates deeper insights into mechanisms of interaction and matrix-strain interactions. Cellular targets of high pressure treatment in E. coli include the barrier properties of the outer membrane, the integrity of the cytoplasmic membrane as well as the activity of membrane-bound enzymes, and the integrity of ribosomes. The pressure-induced denaturation of membrane bound enzymes results in generation of reactive oxygen species and subsequent cell death caused by oxidative stress. Remarkably, pressure resistance at the single cell level relates to the disposition of misfolded proteins in inclusion bodies. While the pressure resistance E. coli can be manipulated by over-expression or deletion of (stress) proteins, the mechanisms of pressure resistance in wild type strains is multi-factorial and not fully understood. This review aims to provide an overview on mechanisms of pressure-mediated cell death in E. coli, and the use of this information for optimization of high pressure processing of foods.

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Differential inactivation of glucose- and glutamate dependent acid resistance of Escherichia coli TMW 2.497 by high-pressure treatments

Cited by 14 publications

References 32 publications

Characterization of a Highly Hop-ResistantLactobacillus brevisStrain Lacking Hop Transport

Characterization of a Highly Hop-ResistantLactobacillus brevisStrain Lacking Hop Transport

Epithelial Cell Extrusion Leads to Breaches in the Intestinal Epithelium

Mechanisms of pressure-mediated cell death and injury in Escherichia coli: from fundamentals to food applications

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