ArticleInfection and immunity2000
Requirement for NF-kappaB in transcriptional activation of monocyte chemotactic protein 1 by Chlamydia pneumoniae in human endothelial cells.
Article in Infection and immunity, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 64 citations in OpenAlex.
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- The suppression of bromodomain and extra-terminal domain inhibits vascular inflammation by blocking NF-κB and MAPK activation.British journal of pharmacology · 2017Article
- Disturbed flow mediated modulation of shear forces on endothelial plane: A proposed model for studying endothelium around atherosclerotic plaques.Scientific reports · 2016Article
- MicroRNA-181b regulates NF-κB-mediated vascular inflammation.The Journal of clinical investigation · 2012Article
- Manipulation of kinase signaling by bacterial pathogens.The Journal of cell biology · 2011Review
- Transcription and translation of human F11R gene are required for an initial step of atherogenesis induced by inflammatory cytokines.Journal of translational medicine · 2011Article
- Cleavage of p65/RelA of the NF-kappaB pathway by Chlamydia.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
- Expression and localization of type III secretion-related proteins of Chlamydia pneumoniae.Medical microbiology and immunology · 2004Article
- Effects of fluoroquinolones on the migration of human phagocytes through Chlamydia pneumoniae-infected and tumor necrosis factor alpha-stimulated endothelial cells.Antimicrobial agents and chemotherapy · 2004Article
- Chlamydia pneumoniae activates epithelial cell proliferation via NF-kappaB and the glucocorticoid receptor.Infection and immunity · 2003Article
- Induction of proinflammatory cytokines in human lung epithelial cells during Chlamydia pneumoniae infection.Infection and immunity · 2003Article
- Induction of the gene encoding macrophage chemoattractant protein 1 by Orientia tsutsugamushi in human endothelial cells involves activation of transcription factor activator protein 1.Infection and immunity · 2002Article
- Helicobacter pylori-induced activation of human endothelial cells.Infection and immunity · 2002Article
- Host-pathogen interactions: subversion and utilization of the NF-kappa B pathway during infection.Infection and immunity · 2002Review
- NF-kappaB family of transcription factors: central regulators of innate and adaptive immune functions.Clinical microbiology reviews · 2002Review
- Chlamydia pneumoniae and Cardiovascular Disease.Current infectious disease reports · 2002Article
- Pathogenesis of atherosclerosis: A multifactorial process.Experimental and clinical cardiology · 2002Article
- Survival of Chlamydia pneumoniae-infected Mono Mac 6 cells is dependent on NF-kappaB binding activity.Infection and immunity · 2001Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Infection with Chlamydia pneumoniae, a causative agent of acute and chronic respiratory diseases, has recently been implicated as a potential risk factor in atherosclerosis. Atherosclerotic lesions are characterized by monocyte infiltration, which may be regulated by the chemokine monocyte chemotactic protein 1 (MCP-1). We have previously shown that C. pneumoniae infection stimulates MCP-1 production in human endothelial cells, an event which may be specific to this species of Chlamydia, since Chlamydia trachomatis infection fails to induce this response. To examine the underlying mechanisms by which C. pneumoniae infection induces MCP-1 production in endothelial cells, the present study investigated the role of transcription factor NF-kappaB in MCP-1 mRNA expression. Human umbilical vein endothelial cells (HUVEC) were infected with the coronary isolate C. pneumoniae A-03 or with C. trachomatis L2, and MCP-1 mRNA expression was assessed after different periods of infection by reverse transcription-PCR. Expression of MCP-1 mRNA in C. pneumoniae-infected HUVEC was significantly elevated as early as 1 h postinfection and increased dramatically by 12 and 24 h compared to baseline controls. Nuclear translocation of NF-kappaB occurred by 30 min of infection, as determined by electrophoretic mobility shift assays and immunofluorescence staining. Treatment of C. pneumoniae-infected HUVEC with parthenolide, a specific inhibitor of NF-kappaB activation, suppressed MCP-1 mRNA expression. In contrast, infection with C. trachomatis L2 did not induce MCP-1 mRNA in infected HUVEC and failed to activate NF-kappaB. Results from this study demonstrate a requirement for NF-kappaB activation in stimulation of MCP-1 gene expression by C. pneumoniae in human endothelial cells. Furthermore, the data suggest that, within the genus Chlamydia, functionally distinct signaling pathways leading to NF-kappaB activation are utilized by C. pneumoniae in endothelial cells during infection.
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