ArticleInfection and immunity2003
Entry of the lymphogranuloma venereum strain of Chlamydia trachomatis into host cells involves cholesterol-rich membrane domains.
Article in Infection and immunity, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 54 citations in OpenAlex.
- Revisiting Pathogen Exploitation of Clathrin-Independent Endocytosis: Mechanisms and Implications.Cells · 2025Review
- Immunosuppressive Mechanisms in Brucellosis in Light of Chronic Bacterial Diseases.Microorganisms · 2022Review
- Otopathogenic Staphylococcus aureus Invades Human Middle Ear Epithelial Cells Primarily through Cholesterol Dependent Pathway.Scientific reports · 2019Article
- Targeting host lipid flows: Exploring new antiviral and antibiotic strategies.Cellular microbiology · 2019Review
- Impact of Dietary Cholesterol on the Pathophysiology of Infectious and Autoimmune Disease.Nutrients · 2018Review
- Genetic variation inProceedings of the National Academy of Sciences of the United States of America · 2018Article
- Human genetic variation inProceedings of the National Academy of Sciences of the United States of America · 2017Article
- Manipulation of Host Cholesterol by Obligate Intracellular Bacteria.Frontiers in cellular and infection microbiology · 2017Review
- Article
- Hijacking and Use of Host Lipids by Intracellular Pathogens.Microbiology spectrum · 2015Review
- Outbreaks of Mycobacterium tuberculosis MDR strains differentially induce neutrophil respiratory burst involving lipid rafts, p38 MAPK and Syk.BMC infectious diseases · 2014Article
- Modulation of host signaling and cellular responses by Chlamydia.Cell communication and signaling : CCS · 2013Review
- Chlamydial intracellular survival strategies.Cold Spring Harbor perspectives in medicine · 2013Review
- Bacterial colonization of host cells in the absence of cholesterol.PLoS pathogens · 2013Article
- RNAi screen of Salmonella invasion shows role of COPI in membrane targeting of cholesterol and Cdc42.Molecular systems biology · 2011Article
- Chlamydial infection of monocytes stimulates IL-1beta secretion through activation of the NLRP3 inflammasome.Microbes and infection · 2010Article
- ApoB-containing lipoproteins promote infectivity of chlamydial species in human hepatoma cell line.World journal of hepatology · 2010Article
- Lipids in host-pathogen interactions: pathogens exploit the complexity of the host cell lipidome.Progress in lipid research · 2010Review
- Comparison of Chlamydia trachomatis serovar L2 growth in polarized genital epithelial cells grown in three-dimensional culture with non-polarized cells.Microbes and infection · 2008Article
- Differences in Chlamydia trachomatis serovar E growth rate in polarized endometrial and endocervical epithelial cells grown in three-dimensional culture.Infection and immunity · 2007Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chlamydiae are bacterial pathogens which develop strictly inside the epithelial cells of their hosts. The mechanism used by chlamydiae to enter cells is not well characterized; however, it is thought to consist of a receptor-mediated process. In addition, the formation of clathrin-coated pits appears to be dispensable for chlamydiae to be internalized by host cells. Clathrin-independent endocytosis has recently been shown to occur through cholesterol-rich lipid microdomains, which are characterized by detergent insolubility. In the present study, we investigated whether these lipid domains play a role in Chlamydia trachomatis serovar L2 internalization by host cells. Our results show that after binding to HeLa cells, chlamydiae are associated with detergent-resistant lipid microdomains (DRMs), which can be isolated by fractionation of infected HeLa cells and flotation on a sucrose gradient. After internalization by HeLa cells, chlamydiae were still found in DRMs. In addition, extraction of plasma membrane cholesterol inhibited infection of HeLa cells by C. trachomatis. Many of the proteins associated with DRMs are glycosylphosphatidylinositol (GPI)-anchored proteins; however, our results could not identify a role for GPI-anchored proteins in the entry process. The same results were obtained for Chlamydia psittaci strain GPIC. We propose that cholesterol-rich domains participate in the entry of chlamydiae into host cells. Chlamydia binding to cholesterol-rich domains may lead to coalescence of the bacterial cells, which could trigger internalization by host cells.
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Registered trials
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