ArticlePloS one2013
Basolateral invasion and trafficking of Campylobacter jejuni in polarized epithelial cells.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 46 citations in OpenAlex.
- Review
- Campylobacter jejuni virulence factors: update on emerging issues and trends.Journal of biomedical science · 2024Review
- Engagement of αFrontiers in microbiology · 2024Article
- Campylobacter jejuni: targeting host cells, adhesion, invasion, and survival.Applied microbiology and biotechnology · 2023Review
- Evolution and Role of Proteases inBiomolecules · 2023Review
- Article
- The ALPK1 pathway drives the inflammatory response to Campylobacter jejuni in human intestinal epithelial cells.PLoS pathogens · 2021Article
- Article
- Campylobacter Virulence Factors and Molecular Host-Pathogen Interactions.Current topics in microbiology and immunology · 2021Review
- Invasion and trafficking of hypervirulent group B streptococci in polarized enterocytes.PloS one · 2021Article
- Molecular Dissection of theMicroorganisms · 2020Article
- Article
- CapC, a Novel Autotransporter and Virulence Factor of Campylobacter jejuni.Applied and environmental microbiology · 2018Article
- Cellular Tight Junctions Prevent EffectiveFrontiers in cellular and infection microbiology · 2018Article
- Chicken Anti-Campylobacter Vaccine - Comparison of Various Carriers and Routes of Immunization.Frontiers in microbiology · 2016Article
- Cultured enterocytes internalise bacteria across their basolateral surface for, pathogen-inhibitable, trafficking to the apical compartment.Scientific reports · 2015Article
- The Campylobacter jejuni RacRS two-component system activates the glutamate synthesis by directly upregulating γ-glutamyltranspeptidase (GGT).Frontiers in microbiology · 2015Article
- Insights into Campylobacter jejuni colonization of the mammalian intestinal tract using a novel mouse model of infection.Gut microbes · 2015Review
- Inflammasome activation by Campylobacter jejuni.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- Peripheral CD4+ T cell cytokine responses following human challenge and re-challenge with Campylobacter jejuni.PloS one · 2014Article
Corrections and comments
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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
Campylobacter jejuni is a major cause of bacterial diarrheal disease. Most enteropathogenic bacteria including C. jejuni can invade cultured eukaryotic cells via an actin- and/or microtubule-dependent and an energy-consuming uptake process. Recently, we identified a novel highly efficient C. jejuni invasion pathway that involves bacterial migration into the subcellular space of non-polarized epithelial cells (termed subvasion) followed by invasion from the cell basis. Here we report cellular requirements of this entry mechanism and the subsequent intracellular trafficking route of C. jejuni in polarized islands of Caco-2 intestinal epithelial cells. Advanced microscopy on infected cells revealed that C. jejuni invades the polarized intestinal cells via the subcellular invasion pathway. Remarkably, invasion was not blocked by the inhibitors of microtubule dynamics colchicine or paclitaxel, and was even enhanced after disruption of host cell actin filaments by cytochalasin D. Invasion also continued after dinitrophenol-induced cellular depletion of ATP, whereas this compound effectively inhibited the uptake of invasive Escherichia coli. Confocal microscopy demonstrated that intracellular C. jejuni resided in membrane-bound CD63-positive cellular compartments for up to 24 h. Establishment of a novel luciferase reporter-based bacterial viability assay, developed to overcome the limitations of the classical bacterial recovery assay, demonstrated that a subset of C. jejuni survived intracellularly for up to 48 h. Taken together, our results indicate that C. jejuni is able to actively invade polarized intestinal epithelial cells via a novel actin- and microtubule-independent mechanism and remains metabolically active in the intracellular niche for up to 48 hours.
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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.