ArticleInfection and immunity2005
Cholesterol-enriched membrane microdomains are required for inducing host cell cytoskeleton rearrangements in response to attaching-effacing Escherichia coli.
Article in Infection and immunity, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed, 32 citations in OpenAlex.
- Lipid larceny: channelizing host lipids for establishing successful pathogenesis by bacteria.Virulence · 2021Review
- Various Facets of Pathogenic Lipids in Infectious Diseases: Exploring Virulent Lipid-Host Interactome and Their Druggability.The Journal of membrane biology · 2020Review
- Endothelial nitric oxide synthase activation is required for heparin receptor effects on vascular smooth muscle cells.American journal of physiology. Cell physiology · 2020Article
- Otopathogenic Staphylococcus aureus Invades Human Middle Ear Epithelial Cells Primarily through Cholesterol Dependent Pathway.Scientific reports · 2019Article
- The Interaction ofFrontiers in cellular and infection microbiology · 2019Article
- Article
- Type Three Secretion System in Attaching and Effacing Pathogens.Frontiers in cellular and infection microbiology · 2016Review
- Hijacking and Use of Host Lipids by Intracellular Pathogens.Microbiology spectrum · 2015Review
- Pore-forming Activity of the Escherichia coli Type III Secretion System Protein EspD.The Journal of biological chemistry · 2015Article
- Protein kinase C mediates enterohemorrhagic Escherichia coli O157:H7-induced attaching and effacing lesions.Infection and immunity · 2014Article
- Article
- Enterohemorrhagic Escherichia coli O157:H7 Shiga toxins inhibit gamma interferon-mediated cellular activation.Infection and immunity · 2012Article
- How cholesterol regulates endothelial biomechanics.Frontiers in physiology · 2012Article
- The N-terminal amphipathic region of the Escherichia coli type III secretion system protein EspD is required for membrane insertion and function.Molecular microbiology · 2011Article
- RNAi screen of Salmonella invasion shows role of COPI in membrane targeting of cholesterol and Cdc42.Molecular systems biology · 2011Article
- Enteropathogenic Escherichia coli, Samonella, Shigella and Yersinia: cellular aspects of host-bacteria interactions in enteric diseases.Gut pathogens · 2010Article
- Role of host cell polarity and leading edge properties in Pseudomonas type III secretion.Microbiology (Reading, England) · 2010Article
- The Bordetella type III secretion system effector BteA contains a conserved N-terminal motif that guides bacterial virulence factors to lipid rafts.Cellular microbiology · 2009Article
- Enteropathogenic Escherichia coli subverts phosphatidylinositol 4,5-bisphosphate and phosphatidylinositol 3,4,5-trisphosphate upon epithelial cell infection.Molecular biology of the cell · 2009Article
- Lipid raft-dependent uptake, signalling and intracellular fate of Porphyromonas gingivalis in mouse macrophages.Cellular microbiology · 2008Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The diarrheal pathogens enterohemorrhagic Escherichia coli (EHEC) O157:H7 strain CL56 and enteropathogenic Escherichia coli (EPEC) O127:H6 strain E2348/69 adhere intimately to epithelial cells through attaching-effacing lesions, which are characterized by rearrangements of the host cytoskeleton, intimate adherence, and destruction of microvilli. These cytoskeletal responses require activation of host signal transduction pathways. Lipid rafts are signaling microdomains enriched in sphingolipid and cholesterol in the plasma membrane. The effect of perturbing plasma membrane cholesterol on bacterial intimate adherence was assessed. Infection of both HEp-2 cells and primary skin fibroblasts with strains CL56 and E2348/69 caused characteristic rearrangements of the cytoskeleton at sites of bacterial adhesion. CL56- and E2348/69-induced cytoskeletal rearrangements were inhibited following cholesterol depletion. Addition of exogenous cholesterol to depleted HEp-2 cells restored cholesterol levels and rescued bacterially induced alpha-actinin mobilization. Quantitative bacterial adherence assays showed that EPEC adherence to HEp-2 cells was dramatically reduced following cholesterol depletion, whereas the adherence of EHEC remained high. Cytoskeletal rearrangements on skin fibroblasts obtained from children with Niemann-Pick type C disease were markedly reduced. These findings indicate that host membrane cholesterol contained in lipid rafts is necessary for the cytoskeletal rearrangements following infection with attaching-effacing Escherichia coli. Differences in initial adherence indicate divergent roles for host membrane cholesterol in the pathogenesis of EHEC and EPEC infections.
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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.