Growth inhibition of Listeria monocytogenes by a nonbacteriocinogenic Carnobacterium piscicola

Aims:  This study elucidates the mechanisms by which a nonbacteriocinogenic Carnobacterium piscicola inhibits growth of Listeria monocytogenes. Methods and Results:  Listeria monocytogenes was exposed to live cultures of a bacteriocin‐negative variant of C. piscicola A9b in co‐culture, in a diffusio...

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Veröffentlicht in:Journal of applied microbiology 2005-01, Vol.98 (1), p.172-183
Hauptverfasser: Nilsson, L., Hansen, T.B., Garrido, P., Buchrieser, C., Glaser, P., Knøchel, S., Gram, L., Gravesen, A.
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container_end_page 183
container_issue 1
container_start_page 172
container_title Journal of applied microbiology
container_volume 98
creator Nilsson, L.
Hansen, T.B.
Garrido, P.
Buchrieser, C.
Glaser, P.
Knøchel, S.
Gram, L.
Gravesen, A.
description Aims:  This study elucidates the mechanisms by which a nonbacteriocinogenic Carnobacterium piscicola inhibits growth of Listeria monocytogenes. Methods and Results:  Listeria monocytogenes was exposed to live cultures of a bacteriocin‐negative variant of C. piscicola A9b in co‐culture, in a diffusion chamber system, and to a cell‐free supernatant. Suppression of maximum cell density (0–3·5 log units) of L. monocytogenes was proportional to initial levels of C. pisciola (103–107 CFU ml−1). Cell‐to‐cell contact was not required to cause inhibition. The cell‐free C. piscicola supernatant caused a decrease in L. monocytogenes maximum cell density, which was abolished by glucose addition but not by amino acid, vitamin or mineral addition. The fermentate also gave rise to a longer lag phase and a reduction in growth rate. These effects were independent of glucose and may have been caused by acetate production by C. piscicola. 2D gel‐electrophoretic patterns of L. monocytogenes exposed to C. piscicola or to L. monocytogenes fermentate did not differ. Treatment with C. piscicola fermentate resulted in down‐regulation (twofold) of genes involved in purine‐ or pyrimidine metabolism, and up‐regulation (twofold) of genes from the regulon for vitamin B12 biosynthesis and propanediol and ethanolamine utilization. Conclusions:  A nonbacteriocinogenic C. piscicola reduced growth of L. monocytogenes partly by glucose depletion. Significance and Impact of the Study:  Understanding the mechanism of microbial interaction enhances prediction of growth in mixed communities as well as use of bioprotective principles for food preservation.
doi_str_mv 10.1111/j.1365-2672.2004.02438.x
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Methods and Results:  Listeria monocytogenes was exposed to live cultures of a bacteriocin‐negative variant of C. piscicola A9b in co‐culture, in a diffusion chamber system, and to a cell‐free supernatant. Suppression of maximum cell density (0–3·5 log units) of L. monocytogenes was proportional to initial levels of C. pisciola (103–107 CFU ml−1). Cell‐to‐cell contact was not required to cause inhibition. The cell‐free C. piscicola supernatant caused a decrease in L. monocytogenes maximum cell density, which was abolished by glucose addition but not by amino acid, vitamin or mineral addition. The fermentate also gave rise to a longer lag phase and a reduction in growth rate. These effects were independent of glucose and may have been caused by acetate production by C. piscicola. 2D gel‐electrophoretic patterns of L. monocytogenes exposed to C. piscicola or to L. monocytogenes fermentate did not differ. Treatment with C. piscicola fermentate resulted in down‐regulation (twofold) of genes involved in purine‐ or pyrimidine metabolism, and up‐regulation (twofold) of genes from the regulon for vitamin B12 biosynthesis and propanediol and ethanolamine utilization. Conclusions:  A nonbacteriocinogenic C. piscicola reduced growth of L. monocytogenes partly by glucose depletion. 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Methods and Results:  Listeria monocytogenes was exposed to live cultures of a bacteriocin‐negative variant of C. piscicola A9b in co‐culture, in a diffusion chamber system, and to a cell‐free supernatant. Suppression of maximum cell density (0–3·5 log units) of L. monocytogenes was proportional to initial levels of C. pisciola (103–107 CFU ml−1). Cell‐to‐cell contact was not required to cause inhibition. The cell‐free C. piscicola supernatant caused a decrease in L. monocytogenes maximum cell density, which was abolished by glucose addition but not by amino acid, vitamin or mineral addition. The fermentate also gave rise to a longer lag phase and a reduction in growth rate. These effects were independent of glucose and may have been caused by acetate production by C. piscicola. 2D gel‐electrophoretic patterns of L. monocytogenes exposed to C. piscicola or to L. monocytogenes fermentate did not differ. 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source MEDLINE; Oxford Journals Online; Wiley Blackwell Journals
subjects 2D PAGE
2‐chamber system
Bacteriological Techniques
Biological and medical sciences
carnobacteriocin B2
Carnobacterium piscicola
DNA micro‐arrays
Food Microbiology
Food Preservation
Fundamental and applied biological sciences. Psychology
Glucose - metabolism
glucose competition
Lactobacillus - metabolism
Listeria monocytogenes
Listeria monocytogenes - growth & development
microbial interaction
Microbiology
title Growth inhibition of Listeria monocytogenes by a nonbacteriocinogenic Carnobacterium piscicola
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