ArticleInfection and immunity2001
Survival of Chlamydia pneumoniae-infected Mono Mac 6 cells is dependent on NF-kappaB binding activity.
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 22 papers.
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Who cites it
22 citing papers in PubMed, 61 citations in OpenAlex.
- Article
- Parthenolide and Its Derivatives in the Treatment of Respiratory Tract Diseases: Therapeutic Effects and Molecular Mechanisms.Drug design, development and therapy · 2026Review
- Insights into Chlamydia Development and Host Cells Response.Microorganisms · 2024Review
- Review
- Host cell death during infection with Chlamydia: a double-edged sword.FEMS microbiology reviews · 2021Review
- Coxiella burnetii Inhibits Neutrophil Apoptosis by Exploiting Survival Pathways and Antiapoptotic Protein Mcl-1.Infection and immunity · 2018Article
- Article
- The sst1 resistance locus regulates evasion of type I interferon signaling by Chlamydia pneumoniae as a disease tolerance mechanism.PLoS pathogens · 2013Article
- Analysis of Chlamydia pneumoniae infection in mononuclear cells by reverse transcription-PCR targeted to chlamydial gene transcripts.Medical microbiology and immunology · 2011Article
- Chlamydia pneumoniae inhibits activated human T lymphocyte proliferation by the induction of apoptotic and pyroptotic pathways.Journal of immunology (Baltimore, Md. : 1950) · 2011Article
- Article
- Chlamydia pneumoniae GroEL1 protein is cell surface associated and required for infection of HEp-2 cells.Journal of bacteriology · 2008Article
- Coxiella burnetii inhibits apoptosis in human THP-1 cells and monkey primary alveolar macrophages.Infection and immunity · 2007Article
- The apicomplexan pathogen Neospora caninum inhibits host cell apoptosis in the absence of discernible NF-kappa B activation.Infection and immunity · 2007Article
- Host-Cell Survival and Death During Chlamydia Infection.Current immunology reviews · 2007Article
- Escherichia coli prevents phagocytosis-induced death of macrophages via classical NF-kappaB signaling, a link to T-cell activation.Infection and immunity · 2006Article
- Apoptosis in infectious disease: how bacteria interfere with the apoptotic apparatus.Medical microbiology and immunology · 2006Review
- Modulation of tumor necrosis factor by microbial pathogens.PLoS pathogens · 2006Review
- Chlamydia pneumoniae augments the oxidized low-density lipoprotein-induced death of mouse macrophages by a caspase-independent pathway.Infection and immunity · 2005Article
- Chlamydia pneumoniae activates epithelial cell proliferation via NF-kappaB and the glucocorticoid receptor.Infection and immunity · 2003Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The respiratory tract pathogen Chlamydia pneumoniae has been associated with atherosclerosis. Monocytes are supposed to serve as a vehicle for systemic dissemination of intracellular C. pneumoniae from the lung to the artery vessel wall. We were therefore interested in pathogen-induced cellular events associated with NF-kappaB, a crucial transcription factor for both inflammatory cytokines and antiapoptotic molecules. In this study we demonstrate by electrophoretic mobility shift assay that C. pneumoniae infection of the human monocytic cell line Mono Mac 6 induces activation of NF-kappaB over 48 h, with a maximum level at 1 h postinfection. As shown by supershift assay, the activated NF-kappaB complex consists of the subunits RelA (p65) and NF-kappaB1 (p50). Apoptotic host cells were not detected during the early stages of the infection when maximal activation of NF-kappaB was detected. Pretreatment of Mono Mac 6 with the antioxidant and NF-kappaB inhibitor PDTC (pyrrolidine dithiocarbamate) induced activation of caspase-3 and led to apoptotic cell death. The C. pneumoniae-induced activation of the NF-kappaB complex was reduced by PDTC, which in parallel resulted in an increased apoptosis, as quantified by annexin V labeling and terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling reaction. In the complete absence of activated NF-kappaB, when Mono Mac 6 cells were pretreated with the more potent NF-kappaB inhibitors MG-132 and parthenolide a C. pneumoniae-mediated rescue of cells from induced apoptosis could not be achieved. Our results indicate that activation of NF-kappaB in C. pneumoniae-infected Mono Mac 6 cells is associated with protection of Mono Mac 6 cells against apoptosis and might thereby contribute to systemic spread of the pathogen.
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