ArticleFrontiers in cellular and infection microbiology2014
Exploring the chicken embryo as a possible model for studying Listeria monocytogenes pathogenicity.
Article in Frontiers in cellular and infection microbiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- PrfA, the master virulence regulator of Listeria monocytogenes: structural-functional insights, regulatory architecture, and antivirulence strategies.Molecular biology reports · 2026Review
- Characterization ofFoods (Basel, Switzerland) · 2025Article
- The type III secretion system facilitates systemic infections ofMicrobiology spectrum · 2024Article
- Article
- The Virulence and Infectivity of Listeria monocytogenes Are Not Substantially Altered by Elevated SigB Activity.Infection and immunity · 2023Article
- Role in virulence of phospholipases, listeriolysin O and listeriolysin S from epidemic Listeria monocytogenes using the chicken embryo infection model.Veterinary research · 2018Article
- Attenuating Listeria monocytogenes Virulence by Targeting the Regulatory Protein PrfA.Cell chemical biology · 2016Article
- Using the chicken embryo to assess virulence of Listeria monocytogenes and to model other microbial infections.Nature protocols · 2015Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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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