ArticleInfection and immunity2002
Chlamydia trachomatis induces remodeling of the actin cytoskeleton during attachment and entry into HeLa 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 107 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
107 citing papers in PubMed, 163 citations in OpenAlex.
- Obligatory intracellular bacterium Anaplasma phagocytophilum AnkA regulates actin dynamics and spatiotemporal bacterial release.PLoS pathogens · 2026Article
- Pathogenicity and virulence ofVirulence · 2025Review
- Evidence for a post-invasion role of themBio · 2025Article
- Protein tyrosine phosphatase PTP1B is a positive regulator of the intracellular development ofInfection and immunity · 2025Article
- Complete deletion of theInfection and immunity · 2025Article
- Article
- Revisiting Pathogen Exploitation of Clathrin-Independent Endocytosis: Mechanisms and Implications.Cells · 2025Review
- The N-terminus of theMicrobiology spectrum · 2025Article
- Chlamydia trachomatis invasion: a duet of effectors.Biochemical Society transactions · 2025Review
- The N-terminus of thebioRxiv : the preprint server for biology · 2024Article
- Dynamin-dependent entry of Chlamydia trachomatis is sequentially regulated by the effectors TarP and TmeA.Nature communications · 2024Article
- IgG exacerbates genital chlamydial pathology in females by enhancing pathogenic CD8Scandinavian journal of immunology · 2024Article
- Chlamydial YAP activation in host endocervical epithelial cells mediates pro-fibrotic paracrine stimulation of fibroblasts.mSystems · 2023Article
- Article
- Roles of host SUMOylation in bacterial pathogenesis.Infection and immunity · 2023Review
- Dynamin-dependent entry ofResearch square · 2023Article
- Type III Secretion inMicrobiology and molecular biology reviews : MMBR · 2023Review
- When Bacteria and Viruses Collide: A Tale ofViruses · 2023Review
- Article
- Article
47 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
To elucidate the host cell machinery utilized by Chlamydia trachomatis to invade epithelial cells, we examined the role of the actin cytoskeleton in the internalization of chlamydial elementary bodies (EBs). Treatment of HeLa cells with cytochalasin D markedly inhibited the internalization of C. trachomatis serovar L2 and D EBs. Association of EBs with HeLa cells induced localized actin polymerization at the site of attachment, as visualized by either phalloidin staining of fixed cells or the active recruitment of GFP-actin in viable infected cells. The recruitment of actin to the specific site of attachment was accompanied by dramatic changes in the morphology of cell surface microvilli. Ultrastructural studies revealed a transient microvillar hypertrophy that was dependent upon C. trachomatis attachment, mediated by structural components on the EBs, and cytochalasin D sensitive. In addition, a mutant CHO cell line that does not support entry of C. trachomatis serovar L2 did not display such microvillar hypertrophy following exposure to L2 EBs, which is in contrast to infection with serovar D, to which it is susceptible. We propose that C. trachomatis entry is facilitated by an active actin remodeling process that is induced by the attachment of this pathogen, resulting in distinct microvillar reorganization throughout the cell surface and the formation of a pedestal-like structure at the immediate site of attachment and entry.
Indexed as
Identifiers
What OpenQuestion holds
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.