ArticleInfection and immunity2012
Two strikingly different signaling pathways are induced by meningococcal type IV pili on endothelial and epithelial cells.
Article in Infection and immunity, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed.
- Arf1 is involved in Neisseria meningitidis-induced cortical branched F-actin network reorganization.EMBO reports · 2026Article
- Overexpression of endothelial S1pr2 promotes blood-brain barrier disruption via JNK/c-Jun/MMP-9 pathway after traumatic brain injury in bothFrontiers in pharmacology · 2024Article
- Microevolution and Its Impact on Hypervirulence, Antimicrobial Resistance, and Vaccine Escape inMicroorganisms · 2023Review
- Mechanical Activation of the βFrontiers in endocrinology · 2022Review
- The Host-Pathogen Interactions and Epicellular Lifestyle ofFrontiers in cellular and infection microbiology · 2022Review
- Interactions and Signal Transduction Pathways Involved during Central Nervous System Entry byInternational journal of molecular sciences · 2020Review
- Commensal Neisseria cinerea impairs Neisseria meningitidis microcolony development and reduces pathogen colonisation of epithelial cells.PLoS pathogens · 2020Article
- An ADAM-10 dependent EPCR shedding links meningococcal interaction with endothelial cells to purpura fulminans.PLoS pathogens · 2018Article
- A virulence-associated filamentous bacteriophage of Neisseria meningitidis increases host-cell colonisation.PLoS pathogens · 2017Article
- Targeting the Mucosal Barrier: How Pathogens Modulate the Cellular Polarity Network.Cold Spring Harbor perspectives in biology · 2017Review
- Neisserial Heparin Binding Antigen (NHBA) Contributes to the Adhesion of Neisseria meningitidis to Human Epithelial Cells.PloS one · 2016Article
- Pathogens penetrating the central nervous system: infection pathways and the cellular and molecular mechanisms of invasion.Clinical microbiology reviews · 2014Review
- Pathogenic Neisseria meningitidis utilizes CD147 for vascular colonization.Nature medicine · 2014Article
- Article
- Sigma factor RpoN (σ54) regulates pilE transcription in commensal Neisseria elongata.Molecular microbiology · 2013Article
- The biology of Neisseria adhesins.Biology · 2013Article
- Pathogenesis of meningococcemia.Cold Spring Harbor perspectives in medicine · 2013Review
- The hCMEC/D3 cell line as a model of the human blood brain barrier.Fluids and barriers of the CNS · 2013Article
- β-Arrestins in the immune system.Progress in molecular biology and translational science · 2013Review
- Dual pili post-translational modifications synergize to mediate meningococcal adherence to platelet activating factor receptor on human airway cells.PLoS pathogens · 2013Article
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Following adhesion on brain microvasculature, Neisseria meningitidis is able to cross the blood-brain barrier (BBB) by recruiting the polarity complex and the cell junction proteins, thus allowing the opening of the paracellular route. This feature is the consequence of the activation by the type IV pili of the β2-adrenergic receptor/β-arrestin signaling pathway. Here, we have extended this observation to primary peripheral endothelial cells, and we report that the interaction of N. meningitidis with the epithelium is strikingly different. The recruitment of the junctional components by N. meningitidis is indeed restricted to endothelial cell lines, and no alteration of the cell-cell junctions can be seen in epithelial monolayers following meningococcal type IV pilus-mediated colonization. Consistently, the β2-adrenergic receptor/β-arrestin pathway was not hijacked by bacteria adhering on epithelial cells. In addition, we showed that the consequences of the bacterial signaling on epithelial cells is different from that of endothelial cells, since N. meningitidis-induced signaling which protects the microcolonies from shear stress on endothelial cells is unable to do so on epithelial cells. Finally, we report that the minor pilin PilV, which has been shown to be essential for endothelial cell response, is not a required bacterial determinant to induce an epithelial cell response. These data demonstrate that even though pilus-mediated signaling induces an apparently similar cortical plaque, in epithelial and endothelial cell lineages, the signaling pathways are strikingly different in both models.
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