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Exploring the chicken embryo as a possible model for studying Listeria monocytogenes pathogenicity. | LitMetric

Exploring the chicken embryo as a possible model for studying Listeria monocytogenes pathogenicity.

Front Cell Infect Microbiol

Department of Molecular Biology, Umeå University Umeå, Sweden ; Laboratory for Molecular Infection Medicine Sweden, Umeå University Umeå, Sweden ; Umeå Centre for Microbial Research, Umeå University Umeå, Sweden.

Published: July 2015

AI Article Synopsis

  • Listeria monocytogenes is a harmful bacterium that can lead to serious and often fatal infections in humans.
  • Researchers explored using chicken embryos as a model to study this bacteria, comparing its effects with both a wild-type strain and strains lacking specific virulence factors.
  • Findings indicate that the wild-type strain can kill chicken embryos quickly, while strains missing certain adhesins have similar mortality rates, suggesting the chicken model is useful for studying L. monocytogenes, albeit with differences compared to human infections.

Article Abstract

Listeria monocytogenes is a bacterial pathogen capable of causing severe infections in humans, often with fatal outcomes. Many different animal models exist to study L. monocytogenes pathogenicity, and we have investigated the chicken embryo as an infection model: What are the benefits and possible drawbacks? We have compared a defined wild-type strain with its isogenic strains lacking well-characterized virulence factors. Our results show that wild-type L. monocytogenes, already at a relatively low infection dose (~5 × 10(2) cfu), caused death of the chicken embryo within 36 h, in contrast to strains lacking the main transcriptional activator of virulence, PrfA, or the cytolysin LLO. Surprisingly, strains lacking the major adhesins InlA and InlB caused similar mortality as the wild-type strain. In conclusion, our results suggest that the chicken embryo is a practical model to study L. monocytogenes infections, especially when analyzing alternative virulence pathways independent of the InlA and InlB adhesins. However, the route of infection might be different from a human infection. The chicken embryo model and other Listeria infection models are discussed.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4261823PMC
http://dx.doi.org/10.3389/fcimb.2014.00170DOI Listing

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