ArticleThe Journal of experimental medicine2004
Chlamydia inhibit host cell apoptosis by degradation of proapoptotic BH3-only proteins.
Article in The Journal of experimental medicine, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers.
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
96 citing papers in PubMed, 202 citations in OpenAlex.
- Trial
- Obligate intracellular bacteria and host cell death pathways-the matter of life and death.Cell and tissue research · 2025Review
- Pathogenicity and virulence ofVirulence · 2025Review
- Impacts of penicillin G on Chlamydia trachomatis serovar D and host HeLa cells in genital infections.Archives of microbiology · 2025Article
- The N-terminus of theMicrobiology spectrum · 2025Article
- The possible pathogenic mechanisms of microorganisms in infertility: a narrative review.Archives of microbiology · 2025Review
- Irradiated whole cell Chlamydia vaccine confers significant protection in a murine genital tract challenge model.NPJ vaccines · 2024Article
- The N-terminus of thebioRxiv : the preprint server for biology · 2024Article
- Decoding mitochondrial DNA damage and repair associated withFrontiers in cellular and infection microbiology · 2024Review
- Mitochondrial Dysfunction in Bacterial Infections.Pathogens (Basel, Switzerland) · 2023Review
- Review
- Deregulation of the cyclin-dependent kinase inhibitor p27 as a putative candidate for transformation inAIMS microbiology · 2023Article
- Plasmid-mediated virulence inFrontiers in cellular and infection microbiology · 2023Review
- LncRNA ZEB1-AS1/miR-1224-5p / MAP4K4 axis regulates mitochondria-mediated HeLa cell apoptosis in persistentVirulence · 2022Article
- Chlamydia trachomatis inhibits apoptosis in infected cells by targeting the pro-apoptotic proteins Bax and Bak.Cell death and differentiation · 2022Article
- Chlamydia trachomatis L2/434/Bu Favors Hypoxia for its Growth in Human Lymphoid Jurkat Cells While Maintaining Production of Proinflammatory Cytokines.Current microbiology · 2022Article
- Antibiotics Use and Subsequent Risk of Colorectal Cancer: A Swedish Nationwide Population-Based Study.Journal of the National Cancer Institute · 2022Article
- Manipulation of Host Cell Organelles by Intracellular Pathogens.International journal of molecular sciences · 2021Review
- Host cell death during infection with Chlamydia: a double-edged sword.FEMS microbiology reviews · 2021Review
- Recent Advances on the Innate Immune Response toFrontiers in cellular and infection microbiology · 2021Review
36 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
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chlamydia are obligate intracellular bacteria that replicate in a vacuole inside a host cell. Chlamydial infection has been shown to protect the host cell against apoptotic stimuli. This is likely important for the ability of Chlamydia to reproduce in human cells. Here we show that resistance to apoptosis is conveyed by the destruction of the proapoptotic BH3-only proteins Bim/Bod, Puma, and Bad during infection. Apoptotic stimuli were blocked upstream of the mitochondrial activation of Bax/Bak. During infection with both species, Chlamydia trachomatis and Chlamydia pneumoniae, Bim protein gradually disappeared without noticeable changes in Bim mRNA. The disappearance was blocked by inhibitors of the proteasome. Infected cells retained sensitivity to Bim expressed by transfection, indicating functional relevance of the Bim disappearance. Fusion to Bim targeted the green fluorescent protein for destruction during infection. Analysis of truncation mutants showed that a short region of Bim containing the BH3 domain was sufficient for destruction during chlamydial infection. Like Bim, Puma and Bad proteins disappeared during infection. These results reveal a novel way by which microbes can interfere with the host cell's apoptotic machinery, and provide a molecular explanation of the cellular resistance to apoptosis during infection with Chlamydia.
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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.