ArticleInfection and immunity2015
Intracellular Listeria monocytogenes comprises a minimal but vital fraction of the intestinal burden following foodborne infection.
Article in Infection and immunity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed.
- Heparin-binding enhances extracellular listeriolysin O activity, overcoming cholesterol inhibition and pH dependence.Journal of bacteriology · 2026Article
- Avoidance of MAIT cells is an essential determinant ofProceedings of the National Academy of Sciences of the United States of America · 2026Article
- ReprogrammingmBio · 2026Article
- Histone demethylase JMJD2D promotes macrophage IL-12b expression and contributes to host defense againstFrontiers in cellular and infection microbiology · 2026Article
- Functional cooperation between LIPI-4 and listeriolysin O governs intracellular replication and systemic virulence ofFrontiers in microbiology · 2026Article
- ARHGEF2 Isoform Switching Couples Intestinal Epithelial Barrier Function with Autophagic Response to Pathogens.Research square · 2025Article
- Article
- Review
- A genome-wide screen in ex vivo gallbladders identifies Listeria monocytogenes factors required for virulence in vivo.PLoS pathogens · 2025Article
- Article
- Advancing vaccine technology through the manipulation of pathogenic and commensal bacteria.Materials today. Bio · 2024Review
- Lymph node stromal cells vary in susceptibility to infection but can support the intracellular growth of Listeria monocytogenes.Journal of leukocyte biology · 2024Article
- Apolipoprotein E genotype affects innate susceptibility toInfection and immunity · 2023Article
- A genome-wide screen in macrophages identifies PTEN as required for myeloid restriction of Listeria monocytogenes infection.PLoS pathogens · 2023Article
- Egress of Listeria monocytogenes from Mesenteric Lymph Nodes Depends on Intracellular Replication and Cell-to-Cell Spread.Infection and immunity · 2023Article
- Integrating Network Pharmacology Approaches to Decipher the Multi-Target Pharmacological Mechanism of Microbial Biosurfactants as Novel Green Antimicrobials against Listeriosis.Antibiotics (Basel, Switzerland) · 2022Article
- The use of foodborne infection to evaluate bacterial pathogenesis and host response.Methods in cell biology · 2022Article
- Advances in Irradiated Livestock Vaccine Research and Production Addressing the Unmet Needs for Farmers and Veterinary Services in FAO/IAEA Member States.Frontiers in immunology · 2022Review
- Pathogenicity and virulence ofVirulence · 2021Article
- The redox-responsive transcriptional regulator Rex represses fermentative metabolism and is required for Listeria monocytogenes pathogenesis.PLoS pathogens · 2021Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Listeria monocytogenes is a highly adaptive bacterium that replicates as a free-living saprophyte in the environment as well as a facultative intracellular pathogen that causes invasive foodborne infections. The intracellular life cycle of L. monocytogenes is considered to be its primary virulence determinant during mammalian infection; however, the proportion of L. monocytogenes that is intracellular in vivo has not been studied extensively. In this report, we demonstrate that the majority of wild-type (strain EGDe) and mouse-adapted (InlA(m)-expressing) L. monocytogenes recovered from the mesenteric lymph nodes (MLN) was extracellular within the first few days after foodborne infection. In addition, significantly lower burdens of L. monocytogenes were recovered from the colon, spleen, and liver of gentamicin-treated mice than of control mice. This led us to investigate whether intracellular replication of L. monocytogenes was essential during the intestinal phase of infection. We found that lipoate protein ligase-deficient L. monocytogenes (ΔlplA1) mutants, which display impaired intracellular growth, were able to colonize the colon but did not persist efficiently and had a significant defect in spreading to the MLN, spleen, and liver. Together, these data indicate that the majority of the L. monocytogenes burden in the gastrointestinal tract is extracellular, but the small proportion of intracellular L. monocytogenes is essential for dissemination to the MLN and systemic organs.
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