ArticleInfection and immunity2002
Chlamydia trachomatis disrupts N-cadherin-dependent cell-cell junctions and sequesters beta-catenin in human cervical epithelial cells.
Article in Infection and immunity, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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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.
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Who cites it
29 citing papers in PubMed, 1 synthesis or guideline pooled it, 106 citations in OpenAlex.
- Pooled it
- Wnt/Notch Crosstalk Promotes Epithelial-Mesenchymal Transition DuringMicroorganisms · 2026Article
- Development of a predictive model integrating urogenital pathogens and inflammatory markers for human papillomavirus infection.Frontiers in cellular and infection microbiology · 2026Article
- Molecular Detection of Human Papillomavirus (HPV) and Other Sexually Transmitted Pathogens in Cervical and Self-Collected Specimens.International journal of molecular sciences · 2025Article
- Gynecological Cancers and Microbiota Dynamics: Insights into Pathogenesis and Therapy.International journal of molecular sciences · 2024Review
- Mechanisms of crosstalk between the oropharyngeal microbiome and human papillomavirus in oropharyngeal carcinogenesis: a mini review.Frontiers in oncology · 2024Review
- When Bacteria and Viruses Collide: A Tale ofViruses · 2023Review
- The immunolocalization of cadherins and beta-catenin in the cervix and vagina of cycling cows.Veterinary research communications · 2023Article
- Chlamydia repurposes the actin-binding protein EPS8 to disassemble epithelial tight junctions and promote infection.Cell host & microbe · 2022Article
- Review
- The mitochondrially-localized nucleoside diphosphate kinase D (NME4) is a novel metastasis suppressor.BMC biology · 2021Article
- Host-Pathogen Interactions ofPathogens (Basel, Switzerland) · 2021Article
- Review
- Murine Endometrial Organoids to ModelFrontiers in cellular and infection microbiology · 2020Article
- Article
- A unique insight into the MiRNA profile during genital chlamydial infection.BMC genomics · 2019Article
- A renewed tool kit to exploreF1000Research · 2019Review
- TLR3 deficiency exacerbates the loss of epithelial barrier function during genital tract Chlamydia muridarum infection.PloS one · 2019Article
- Inhibition of Wnt Signaling Pathways ImpairsFrontiers in cellular and infection microbiology · 2017Article
- Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The cadherin/catenin complex serves as an important structural component of adherens junctions in epithelial cells. Under certain conditions, beta-catenin can be released from this complex and interact with transcription factors in the nucleus to stimulate the expression of genes that regulate apoptosis and cell cycle control. While studying the effects of the bacterial pathogen Chlamydia trachomatis on human cervical epithelial cells in culture, we observed that C. trachomatis caused the epithelial cells to separate from each other without detaching from their growing surface. The objective of the present study was to determine if this effect might involve the disruption of the cadherin/catenin complex. Primary cultures of human cervical epithelial cells or HeLa cells were infected with C. trachomatis serovar E. Cadherin-like immunoreactive materials and beta-catenin were visualized by immunofluorescence. Preliminary studies showed that N-cadherin was the primary cadherin expressed in both the primary cultures and the HeLa cells. In noninfected cells, N-cadherin and beta-catenin were colocalized at the intercellular junctional complexes. By contrast, the infected cells showed a marked loss of both N-cadherin and beta-catenin labeling from the junctional complexes and the concomitant appearance of intense beta-catenin labeling associated with the chlamydial inclusion. The results of Western blot analyses of extracts of C. trachomatis showed no evidence of cross-reactivity with the beta-catenin antibody. These results indicate that C. trachomatis causes the breakdown of the N-cadherin/beta-catenin complex and that the organism can sequester beta-catenin within the chlamydial inclusion. This could represent an important mechanism by which C. trachomatis alters epithelial cell function.
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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.