ArticleJournal of clinical immunology2008
Host defenses to Rickettsia rickettsii infection contribute to increased microvascular permeability in human cerebral endothelial cells.
Article in Journal of clinical immunology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed, 56 citations in OpenAlex.
- The host calcium system contributes to intracellularInfection and immunity · 2025Article
- Article
- Benidipine impairs innate immunity converting sublethal to lethal infections in a murine model of spotted fever rickettsiosis.PLoS neglected tropical diseases · 2024Article
- Spotted fever rickettsia-induced microvascular endothelial barrier dysfunction is delayed by the calcium channel blocker benidipine.Biochemical and biophysical research communications · 2023Article
- Mechanical Forces Govern Interactions of Host Cells with Intracellular Bacterial Pathogens.Microbiology and molecular biology reviews : MMBR · 2022Review
- Rickettsia conorii infection with fatal complication.Autopsy & case reports · 2022Article
- Microvascular Angiopathic Consequences of COVID-19.Frontiers in cardiovascular medicine · 2021Review
- Neuroinflammation associated with scrub typhus and spotted fever group rickettsioses.PLoS neglected tropical diseases · 2020Review
- Pathogenesis of Rickettsial Diseases: Pathogenic and Immune Mechanisms of an Endotheliotropic Infection.Annual review of pathology · 2019Review
- Bacterial Manipulation of Wnt Signaling: A Host-Pathogen Tug-of-Wnt.Frontiers in immunology · 2019Review
- A Concise Review of the Epidemiology and Diagnostics of Rickettsioses: Rickettsia and Orientia spp.Journal of clinical microbiology · 2018Review
- Enhancer Associated Long Non-coding RNA Transcription and Gene Regulation in Experimental Models of Rickettsial Infection.Frontiers in immunology · 2018Article
- Persisting Rickettsia typhi Causes Fatal Central Nervous System Inflammation.Infection and immunity · 2016Article
- Article
- Compartmentalized, functional role of angiogenin during spotted fever group rickettsia-induced endothelial barrier dysfunction: evidence of possible mediation by host tRNA-derived small noncoding RNAs.BMC infectious diseases · 2013Article
- Contribution of NK cells to the innate phase of host protection against an intracellular bacterium targeting systemic endothelium.The American journal of pathology · 2012Article
- Rickettsiae induce microvascular hyperpermeability via phosphorylation of VE-cadherins: evidence from atomic force microscopy and biochemical studies.PLoS neglected tropical diseases · 2012Article
- 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
- Nitric oxide/cGMP signalling induces Escherichia coli K1 receptor expression and modulates the permeability in human brain endothelial cell monolayers during invasion.Cellular microbiology · 2010Article
- Infection of the endothelium by members of the order Rickettsiales.Thrombosis and haemostasis · 2009Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Rickettsiae are arthropod-borne intracellular bacterial pathogens that primarily infect the microvascular endothelium leading to systemic spread of the organisms and the major pathophysiological effect, increased microvascular permeability, and edema in vital organs such as the lung and brain. Much work has been done on mechanisms of immunity to rickettsiae, as well as the responses of endothelial cells to rickettsial invasion. However, to date, no one has described the mechanisms of increased microvascular permeability during acute rickettsiosis. We sought to establish an in vitro model of human endothelial-target rickettsial infection using the etiological agent of Rocky Mountain spotted fever, Rickettsia rickettsii, and human cerebral microvascular endothelial cells. Endothelial cells infected with R. rickettsii exhibited a dose-dependent decrease in trans-endothelial electrical resistance, which translates into increased monolayer permeability. Additionally, we showed that the addition of pro-inflammatory stimuli essential to rickettsial immunity dramatically enhanced this effect. This increase in permeability correlates with dissociation of adherens junctions between endothelial cells and is not dependent on the presence of nitric oxide. Taken together, these results demonstrate for the first time that increased microvascular permeability associated with rickettsial infection is partly attributable to intracellular rickettsiae and partly attributable to the immune defenses that have evolved to protect the host from rickettsial spread.
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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.