ArticlePLoS pathogens2011
The pore-forming toxin listeriolysin O mediates a novel entry pathway of L. monocytogenes into human hepatocytes.
Article in PLoS pathogens, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.
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Who cites it
84 citing papers in PubMed, 130 citations in OpenAlex.
- On the role of cell chaining in the attenuation of aVirulence · 2026Article
- Internalization ofAnnals of medicine · 2026Review
- Heparin-binding enhances extracellular listeriolysin O activity, overcoming cholesterol inhibition and pH dependence.Journal of bacteriology · 2026Article
- Recombinant listeriolysin-O as a platform for next-generation vaccines: Mechanisms, immunological evidence, and translational applications in human and veterinary medicine.Open veterinary journal · 2026Review
- Liposomal Nanotraps NeutralizeInfectious microbes & diseases · 2025Article
- An antibody-toxin conjugate targeting CD47 linked to the bacterial toxin listeriolysin O for cancer immunotherapy.Nature cancer · 2025Article
- Comparative Analysis ofMicroorganisms · 2025Article
- TMEM16F Expressed in Kupffer Cells Regulates Liver Inflammation and Metabolism to Protect Against Listeria Monocytogenes.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- The septin cytoskeleton is required for plasma membrane repair.EMBO reports · 2024Article
- The chaperone PrsA2 regulates the secretion, stability, and folding of listeriolysin O duringmBio · 2024Article
- The mitochondrial carboxylase PCCA interacts withApplied and environmental microbiology · 2024Article
- Linalool Reduces Virulence and Tolerance to Adverse Conditions ofAntibiotics (Basel, Switzerland) · 2024Article
- Article
- Roles of host SUMOylation in bacterial pathogenesis.Infection and immunity · 2023Review
- The Application of Cinnamon Twig Extract as an Inhibitor of Listeriolysin O againstMolecules (Basel, Switzerland) · 2023Article
- Genomic and pathogenicity islands ofFrontiers in molecular biosciences · 2023Review
- Live-cell imaging reveals single-cell and population-level infection strategies ofFrontiers in immunology · 2023Article
- Review
- Pneumolysin boosts the neuroinflammatory response to Streptococcus pneumoniae through enhanced endocytosis.Nature communications · 2022Article
- Membrane Cholesterol Content and Lipid Organization Influence Melittin and Pneumolysin Pore-Forming Activity.Toxins · 2022Article
24 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
Abstract
Intracellular pathogens have evolved diverse strategies to invade and survive within host cells. Among the most studied facultative intracellular pathogens, Listeria monocytogenes is known to express two invasins-InlA and InlB-that induce bacterial internalization into nonphagocytic cells. The pore-forming toxin listeriolysin O (LLO) facilitates bacterial escape from the internalization vesicle into the cytoplasm, where bacteria divide and undergo cell-to-cell spreading via actin-based motility. In the present study we demonstrate that in addition to InlA and InlB, LLO is required for efficient internalization of L. monocytogenes into human hepatocytes (HepG2). Surprisingly, LLO is an invasion factor sufficient to induce the internalization of noninvasive Listeria innocua or polystyrene beads into host cells in a dose-dependent fashion and at the concentrations produced by L. monocytogenes. To elucidate the mechanisms underlying LLO-induced bacterial entry, we constructed novel LLO derivatives locked at different stages of the toxin assembly on host membranes. We found that LLO-induced bacterial or bead entry only occurs upon LLO pore formation. Scanning electron and fluorescence microscopy studies show that LLO-coated beads stimulate the formation of membrane extensions that ingest the beads into an early endosomal compartment. This LLO-induced internalization pathway is dynamin-and F-actin-dependent, and clathrin-independent. Interestingly, further linking pore formation to bacteria/bead uptake, LLO induces F-actin polymerization in a tyrosine kinase-and pore-dependent fashion. In conclusion, we demonstrate for the first time that a bacterial pathogen perforates the host cell plasma membrane as a strategy to activate the endocytic machinery and gain entry into the host cell.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.