ArticleInfection and immunity2001
Characterization of antiapoptotic activities of Chlamydia pneumoniae in human cells.
Article in Infection and immunity, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 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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Who cites it
47 citing papers in PubMed, 115 citations in OpenAlex.
- Obligate intracellular bacteria and host cell death pathways-the matter of life and death.Cell and tissue research · 2025Review
- Review
- Chlamydia trachomatis inhibits apoptosis in infected cells by targeting the pro-apoptotic proteins Bax and Bak.Cell death and differentiation · 2022Article
- Host cell death during infection with Chlamydia: a double-edged sword.FEMS microbiology reviews · 2021Review
- Article
- Microbial uptake by the respiratory epithelium: outcomes for host and pathogen.FEMS microbiology reviews · 2019Review
- Anti-Inflammatory Effect of Feiyangchangweiyan Capsule on Rat Pelvic Inflammatory Disease through JNK/NF-Evidence-based complementary and alternative medicine : eCAM · 2018Article
- Prediction ofSaudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2017Article
- Chlamydia trachomatis Cellular Exit Alters Interactions with Host Dendritic Cells.Infection and immunity · 2017Article
- An epistatic effect of apaf-1 and caspase-9 on chlamydial infection.Apoptosis : an international journal on programmed cell death · 2015Article
- Statistical genetic analysis of serological measures of common, chronic infections in Alaska Native participants in the GOCADAN study.Genetic epidemiology · 2013Article
- Chlamydial intracellular survival strategies.Cold Spring Harbor perspectives in medicine · 2013Review
- The sst1 resistance locus regulates evasion of type I interferon signaling by Chlamydia pneumoniae as a disease tolerance mechanism.PLoS pathogens · 2013Article
- Innate immune responses to Chlamydia pneumoniae infection: role of TLRs, NLRs, and the inflammasome.Microbes and infection · 2012Review
- CPAF: a Chlamydial protease in search of an authentic substrate.PLoS pathogens · 2012Article
- Review: apoptotic mechanisms in bacterial infections of the central nervous system.Frontiers in immunology · 2012Article
- Lack of effective anti-apoptotic activities restricts growth of Parachlamydiaceae in insect cells.PloS one · 2012Article
- Evolutionary conservation of infection-induced cell death inhibition among Chlamydiales.PloS one · 2011Article
- Interactions between bacterial pathogens and mitochondrial cell death pathways.Nature reviews. Microbiology · 2010Review
- Role of high-mobility group box 1 protein and poly(ADP-ribose) polymerase 1 degradation in Chlamydia trachomatis-induced cytopathicity.Infection and immunity · 2010Article
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
No grant is acknowledged in the PubMed record.
Abstract
Chlamydia pneumoniae is an obligate intracellular bacterium which frequently causes airway infection in humans and has been implicated in atherosclerosis. Here we show that infection with C. pneumoniae protects HeLa human epithelioid cells against apoptosis induced by external stimuli. In infected HeLa cells, apoptosis induced by staurosporine and CD95-death-receptor signaling was strongly reduced. Upon treatment with staurosporine, generation of effector caspase activity, processing of caspase-3 and caspase-9 and cytochrome c redistribution were all profoundly inhibited in cells infected with C. pneumoniae. Bacterial protein synthesis during early infection was required for this inhibition. Furthermore, cytochrome c-induced processing and activation of caspases were inhibited in cytosolic extracts from infected cells, suggesting that a C. pneumoniae-dependent antiapoptotic factor was generated in the cytosol upon infection. Infection with C. pneumoniae failed to induce significant NF-kappaB activation in HeLa cells, indicating that no NF-kappaB-dependent cellular factors were involved in the protection against apoptosis. These results show that C. pneumoniae is capable of interfering with the host cell's apoptotic apparatus at probably at least two steps in signal transduction and might explain the propensity of these bacteria to cause chronic infections in humans.
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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.