ArticleBMC microbiology2009
Helicobacter pylori lipopolysaccharide modification, Lewis antigen expression, and gastric colonization are cholesterol-dependent.
Article in BMC microbiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed, 42 citations in OpenAlex.
- Repurposing azole antifungals as rapid bactericidal, membrane-disruptive therapeutics againstMicrobiology spectrum · 2026Article
- Cholesterol sulfate signaling facilitates persistent colonization of mucoid-coccoid H. pylori in gastric environment.International microbiology : the official journal of the Spanish Society for Microbiology · 2026Article
- Co-Occurrence ofBiomedicines · 2025Review
- Statins, Allies against Antibiotic Resistance?Current medicinal chemistry · 2025Review
- A novel salt-tolerant GH42 β-galactosidase with transglycosylation activity from deep-sea metagenome.World journal of microbiology & biotechnology · 2022Article
- Lipid larceny: channelizing host lipids for establishing successful pathogenesis by bacteria.Virulence · 2021Review
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- Unveiling the Crucial Role of Type IV Secretion System and Motility ofFrontiers in immunology · 2020Article
- Helicobacter pylori lipids can form ordered membrane domains (rafts).Biochimica et biophysica acta. Biomembranes · 2019Article
- Otopathogenic Staphylococcus aureus Invades Human Middle Ear Epithelial Cells Primarily through Cholesterol Dependent Pathway.Scientific reports · 2019Article
- The Possible Role ofFrontiers in oncology · 2019Review
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- Stomaching the Possibility of a Pathogenic Role for Helicobacter pylori in Parkinson's Disease.Journal of Parkinson's disease · 2018Review
- Comparison of lipopolysaccharides composition of two different strains of Helicobacter pylori.BMC microbiology · 2017Article
- Co-infections with liver fluke and Helicobacter species: A paradigm change in pathogenesis of opisthorchiasis and cholangiocarcinoma?Parasitology international · 2017Review
- AFrontiers in cellular and infection microbiology · 2017Article
- Cholesterol lipids and cholesterol-containing lipid rafts in bacteria.Chemistry and physics of lipids · 2016Review
- Hijacking and Use of Host Lipids by Intracellular Pathogens.Microbiology spectrum · 2015Review
- Cholesterol suppresses antimicrobial effect of statins.Iranian journal of basic medical sciences · 2015Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
backgroundHelicobacter pylori specifically takes up cholesterol and incorporates it into the bacterial membrane, yet little is currently known about cholesterol's physiological roles. We compared phenotypes and in vivo colonization ability of H. pylori grown in a defined, serum-free growth medium, F12 with 1 mg/ml albumin containing 0 to 50 mug/ml cholesterol.
resultsWhile doubling times were largely unaffected by cholesterol, other overt phenotypic changes were observed. H. pylori strain SS1 grown in defined medium with cholesterol successfully colonized the stomach of gerbils, whereas SS1 grown without cholesterol failed to colonize. H. pylori lipopolysaccharide often displays Lewis X and/or Y antigens. Expression of these antigens measured by whole-cell ELISA was markedly enhanced in response to growth of strain SS1, 26695, or G27 in cholesterol. In addition, electrophoretic analysis of lipopolysaccharide in wild type G27 and in mutants lacking the O-chain revealed structural changes within the oligosaccharide core/lipid A moieties. These responses in Lewis antigen levels and in lipopolysaccharide profiles to cholesterol availability were highly specific, because no changes took place when cholesterol was substituted by beta-sitosterol or bile salts. Disruption of the genes encoding cholesterol alpha-glucosyltransferase or lipid A phosphoethanolamine transferase had no effect on Lewis expression, nor on lipopolysaccharide profiles, nor on the cholesterol responsiveness of these properties. Disruption of the lipid A 1-phosphatase gene eliminated the effect of cholesterol on lipopolysaccharide profiles but not its effect on Lewis expression.
conclusionsTogether these results suggest that cholesterol depletion leads to aberrant forms of LPS that are dependent upon dephosphorylation of lipid A at the 1-position. A tentative model for the observed effects of cholesterol is discussed in which sequential steps of lipopolysaccharide biogenesis and, independently, presentation of Lewis antigen at the cell surface, depend upon membrane composition. These new findings demonstrate that cholesterol availability permits H. pylori to modify its cell envelope in ways that can impact colonization of host tissue in vivo.
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Registered trials
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