ArticleThe Journal of experimental medicine2015
PI3-kinase activation is critical for host barrier permissiveness to Listeria monocytogenes.
Article in The Journal of experimental medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
39 citing papers in PubMed, 72 citations in OpenAlex.
- Coupling Far-Western Blotting with Peptide Microarrays Reveals Novel E-Cadherin Spore-Surface Ligands inJournal of proteome research · 2026Article
- Article
- The PI3K/Akt Pathway in Herpesvirus Biology: A Double-Edged Sword in Host-Virus Interactions.Microorganisms · 2026Review
- Pyruvate-GPR31 axis induces LysoDC dendrite protrusion to M-cell pockets for effective immune responses.Gut microbes · 2025Article
- Listeriosis.Nature reviews. Disease primers · 2025Review
- Goblet cell breakdown: transcriptomics reveals Acinetobacter baumannii early and robust inflammatory response in differentiated human bronchial epithelial cells.Journal of biomedical science · 2025Article
- Engineered Probiotic-Based Biomaterials for Inflammatory Bowel Disease Treatment.Theranostics · 2025Review
- Caveolin-Mediated Endocytosis: Bacterial Pathogen Exploitation and Host-Pathogen Interaction.Cells · 2024Review
- Article
- Redistribution of the Novel Clostridioides difficile Spore Adherence Receptor E-Cadherin by TcdA and TcdB Increases Spore Binding to Adherens Junctions.Infection and immunity · 2023Article
- Review
- Article
- Article
- Pathogenicity and virulence ofVirulence · 2021Article
- Bacterial Biofilms and Their Implications in Pathogenesis and Food Safety.Foods (Basel, Switzerland) · 2021Review
- Foxo1 controls gut homeostasis and commensalism by regulating mucus secretion.The Journal of experimental medicine · 2021Article
- Glucose Decoration on Wall Teichoic Acid Is Required for Phage Adsorption and InlB-Mediated Virulence in Listeria ivanovii.Journal of bacteriology · 2021Article
- Cardiotropic Isolates of Listeria monocytogenes with Enhanced Vertical Transmission Dependent upon the Bacterial Surface Protein InlB.Infection and immunity · 2021Article
- Article
- Maternal-neonatal listeriosis.Virulence · 2020Review
Corrections and comments
- Commented on by
Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Invasion of nonphagocytic cells, a critical property of Listeria monocytogenes (Lm) that enables it to cross host barriers, is mediated by the interaction of two bacterial surface proteins, InlA and InlB, with their respective receptors E-cadherin and c-Met. Although InlA-E-cadherin interaction is necessary and sufficient for Lm crossing of the intestinal barrier, both InlA and InlB are required for Lm crossing of the placental barrier. The mechanisms underlying these differences are unknown. Phosphoinositide 3-kinase (PI3-K) is involved in both InlA- and InlB-dependent pathways. Indeed, InlA-dependent entry requires PI3-K activity but does not activate it, whereas InlB-c-Met interaction activates PI3-K. We show that Lm intestinal target cells exhibit a constitutive PI3-K activity, rendering InlB dispensable for InlA-dependent Lm intestinal barrier crossing. In contrast, the placental barrier does not exhibit constitutive PI3-K activity, making InlB necessary for InlA-dependent Lm placental invasion. Here, we provide the molecular explanation for the respective contributions of InlA and InlB to Lm host barrier invasion, and reveal the critical role of InlB in rendering cells permissive to InlA-mediated invasion. This study shows that PI3-K activity is critical to host barrier permissiveness to microbes, and that pathogens exploit both similarities and differences of host barriers to disseminate.
Indexed as
Identifiers
What OpenQuestion holds
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.