ArticleInfection and immunity1997
Rickettsia rickettsii infection of cultured human endothelial cells induces NF-kappaB activation.
Article in Infection and immunity, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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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
32 citing papers in PubMed, 71 citations in OpenAlex.
- Clinical characteristics and epidemiological analysis of 23 cases of tick-borne rickettsiosis in Xinjiang Uygur Autonomous Region.Frontiers in cellular and infection microbiology · 2026Article
- The host calcium system contributes to intracellularInfection and immunity · 2025Article
- Article
- Signatures in in vitro infection of NSC-34 mouse neurons and their cell nucleus with Rickettsia helvetica.BMC microbiology · 2023Article
- Endothelial Cells as a Key Cell Type for Innate Immunity: A Focused Review on RIG-I Signaling Pathway.Frontiers in immunology · 2022Review
- Mediterranean Spotted Fever: Current Knowledge and Recent Advances.Tropical medicine and infectious disease · 2021Review
- The Many Faces of Bacterium-Endothelium Interactions during Systemic Infections.Microbiology spectrum · 2019Review
- Pathogenesis of Rickettsial Diseases: Pathogenic and Immune Mechanisms of an Endotheliotropic Infection.Annual review of pathology · 2019Review
- Immune response against rickettsiae: lessons from murine infection models.Medical microbiology and immunology · 2017Review
- Suppressor of cytokine signalling protein SOCS1 and UBP43 regulate the expression of type I interferon-stimulated genes in human microvascular endothelial cells infected with Rickettsia conorii.Journal of medical microbiology · 2013Article
- New insight into immunity and immunopathology of Rickettsial diseases.Clinical & developmental immunology · 2012Review
- Beta interferon-mediated activation of signal transducer and activator of transcription protein 1 interferes with Rickettsia conorii replication in human endothelial cells.Infection and immunity · 2011Article
- Rickettsia rickettsii infection of human macrovascular and microvascular endothelial cells reveals activation of both common and cell type-specific host response mechanisms.Infection and immunity · 2010Article
- Infection of the endothelium by members of the order Rickettsiales.Thrombosis and haemostasis · 2009Review
- Host-cell interactions with pathogenic Rickettsia species.Future microbiology · 2009Review
- Infection of human endothelial cells with spotted Fever group rickettsiae stimulates cyclooxygenase 2 expression and release of vasoactive prostaglandins.Infection and immunity · 2006Article
- Invasive phenotype of Candida albicans affects the host proinflammatory response to infection.Infection and immunity · 2005Article
- Changes in the adherens junctions of human endothelial cells infected with spotted fever group rickettsiae.Virchows Archiv : an international journal of pathology · 2005Article
- NF-kappaB activation during Rickettsia rickettsii infection of endothelial cells involves the activation of catalytic IkappaB kinases IKKalpha and IKKbeta and phosphorylation-proteolysis of the inhibitor protein IkappaBalpha.Infection and immunity · 2005Article
- Expression of CX3CL1 (fractalkine) in mice with endothelial-target rickettsial infection of the spotted-fever group.Virchows Archiv : an international journal of pathology · 2005Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Rickettsia rickettsii, the etiologic agent of Rocky Mountain spotted fever, is an obligate intracellular bacterial organism that infects primarily the vascular endothelial cells (EC). A component of the EC response to infection is transcriptional activation, which may contribute to the thrombotic and inflammatory consequences of disease. In this study, we explore R. rickettsii-induced activation of the nuclear factor-kappaB/Rel (NF-kappaB) family of transcription factors involved in early transcriptional responses to injurious stimuli. Two NF-kappaB species were activated by infection and reacted with a double-stranded oligonucleotide probe corresponding to the kappaB binding domain of the murine kappa light-chain gene enhancer. Gel supershift analysis demonstrated the reactivity of these complexes with antibodies against p65 and p50, and the induced species were tentatively identified as p50-p50 homodimers and p50-p65 heterodimers. Semiquantitative reverse transcription-PCR analysis revealed dramatic increases in the steady-state levels of mRNA coding for the inhibitory subunit of NF-kappaB (IkappaB alpha), transcription of which is enhanced by the binding of NF-kappaB within the IkappaB alpha promoter region. NF-kappaB activation was first detected 1.5 h following infection and was biphasic, with an early peak of activation at approximately 3 h, a return to baseline levels at 14 h, and even higher levels of activation at 24 h. It is likely that NF-kappaB activation requires cellular uptake of R. rickettsii, since treatment of EC with cytochalasin B during infection to block entry inhibited activation by only 70% at 3 h. R. rickettsii-induced activation of NF-kappaB may be an important controlling factor in the transcriptional responses of EC to infection with this obligate intracellular organism.
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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.