ArticlePLoS pathogens2013
Pilus phase variation switches gonococcal adherence to invasion by caveolin-1-dependent host cell signaling.
Article in PLoS pathogens, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 25 citations in OpenAlex.
- Article
- The Multifaceted Role of Calcium Signaling in Regulated Necrosis.Biomolecules · 2025Review
- Caveolin-Mediated Endocytosis: Bacterial Pathogen Exploitation and Host-Pathogen Interaction.Cells · 2024Review
- Pathophysiology and Evolving Treatment Options of Septic Arthritis: A Narrative Review.Cureus · 2024Review
- Review
- Gonococcal OMV-delivered PorB induces epithelial cell mitophagy.Nature communications · 2024Article
- Gonococcal invasion into epithelial cells depends on both cell polarity and ezrin.PLoS pathogens · 2021Article
- A Role of Sphingosine in the Intracellular Survival ofFrontiers in cellular and infection microbiology · 2020Article
- Caveolae as Potential Hijackable Gates in Cell Communication.Frontiers in cell and developmental biology · 2020Review
- Folliculin Controls the Intracellular Survival and Trans-Epithelial Passage ofFrontiers in cellular and infection microbiology · 2020Article
- Selection for a CEACAM receptor-specific binding phenotype during Neisseria gonorrhoeae infection of the human genital tract.Infection and immunity · 2015Article
- Rab5 is required in metastatic cancer cells for Caveolin-1-enhanced Rac1 activation, migration and invasion.Journal of cell science · 2014Article
- Bacterial genome instability.Microbiology and molecular biology reviews : MMBR · 2014Review
- Transcriptional landscape and essential genes of Neisseria gonorrhoeae.Nucleic acids research · 2014Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Many pathogenic bacteria cause local infections but occasionally invade into the blood stream, often with fatal outcome. Very little is known about the mechanism underlying the switch from local to invasive infection. In the case of Neisseria gonorrhoeae, phase variable type 4 pili (T4P) stabilize local infection by mediating microcolony formation and inducing anti-invasive signals. Outer membrane porin PorB(IA), in contrast, is associated with disseminated infection and facilitates the efficient invasion of gonococci into host cells. Here we demonstrate that loss of pili by natural pilus phase variation is a prerequisite for the transition from local to invasive infection. Unexpectedly, both T4P-mediated inhibition of invasion and PorB(IA)-triggered invasion utilize membrane rafts and signaling pathways that depend on caveolin-1-Y14 phosphorylation (Cav1-pY14). We identified p85 regulatory subunit of PI3 kinase (PI3K) and phospholipase Cγ1 as new, exclusive and essential interaction partners for Cav1-pY14 in the course of PorBIA-induced invasion. Active PI3K induces the uptake of gonococci via a new invasion pathway involving protein kinase D1. Our data describe a novel route of bacterial entry into epithelial cells and offer the first mechanistic insight into the switch from local to invasive gonococcal infection.
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