ArticleCellular microbiology2013
Neisseria gonorrhoeae breaches the apical junction of polarized epithelial cells for transmigration by activating EGFR.
Article in Cellular microbiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 39 citations in OpenAlex.
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- Three-dimensional models of the cervicovaginal epithelia to study host-microbiome interactions and sexually transmitted infections.Pathogens and disease · 2022Article
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- Gonococcal invasion into epithelial cells depends on both cell polarity and ezrin.PLoS pathogens · 2021Article
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- Folliculin Controls the Intracellular Survival and Trans-Epithelial Passage ofFrontiers in cellular and infection microbiology · 2020Article
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- Neisseria gonorrhoeae infects the heterogeneous epithelia of the human cervix using distinct mechanisms.PLoS pathogens · 2019Article
- MeningiticPathogens (Basel, Switzerland) · 2019Article
- Pathogenic Mannheimia haemolytica Invades Differentiated Bovine Airway Epithelial Cells.Infection and immunity · 2019Article
- Biomimetic Human Tissue Model for Long-Term Study ofFrontiers in microbiology · 2019Article
- Pathogenesis ofFrontiers in immunology · 2018Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Neisseria gonorrhoeae initiates infection at the apical surface of columnar endocervical epithelial cells in the female reproductive tract. These cells provide a physical barrier against pathogens by forming continuous apical junctional complexes between neighbouring cells. This study examines the interaction of gonococci (GC) with polarized epithelial cells. We show that viable GC preferentially localize at the apical side of the cell-cell junction in polarized endometrial and colonic epithelial cells, HEC-1-B and T84. In GC-infected cells, continuous apical junctional complexes are disrupted, and the junction-associated protein β-catenin is redistributed from the apical junction to the cytoplasm and to GC adherent sites; however, overall cellular levels remain unchanged. This redistribution of junctional proteins is associated with a decrease in the 'fence' function of the apical junction but not its 'gate' function. Disruption of the apical junction by removing calcium increases GC transmigration across the epithelial monolayer. GC inoculation induces the phosphorylation of both epidermal growth factor receptor (EGFR) and β-catenin, while inhibition of EGFR kinase activity significantly reduces both GC-induced β-catenin redistribution and GC transmigration. Therefore, the gonococcus is capable of weakening the apical junction and polarity of epithelial cells by activating EGFR, which facilitates GC transmigration across the epithelium.
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Registered trials
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