Evidence map›Paper›PMID 21464244›Full record

ArticleAntimicrobial agents and chemotherapy2011

Cholesterol enhances Helicobacter pylori resistance to antibiotics and LL-37.

David J McGee, Alika E George, Elizabeth A Trainor, Katherine E Horton, Ellen Hildebrandt, Traci L Testerman

Abstract read
In one paragraph

Article in Antimicrobial agents and chemotherapy, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

62 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Trial
  3. Article
  4. Article
  5. 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 · 2026
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  6. Article
  7. Statins, Allies against Antibiotic Resistance?Current medicinal chemistry · 2025
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  8. Article
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  10. Chaenomelin, a New Phenolic Glycoside, and Anti-Plants (Basel, Switzerland) · 2024
    Article
  11. Review
  12. Article
  13. Article
  14. Chemical Investigation ofACS omega · 2022
    Article
  15. Article
  16. Article
  17. Role of lipid rafts in persistentAnnals of translational medicine · 2022
    Review
  18. First Chemical Investigation of Korean Wild Mushroom,Pharmaceuticals (Basel, Switzerland) · 2022
    Article
  19. Two New Fatty Acid Derivatives, Omphalotols A and B and Anti-Pharmaceuticals (Basel, Switzerland) · 2022
    Article
  20. Article

2 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

David J McGeeDepartment of Microbiology and Immunology MSB 2-225, Louisiana State University Health Sciences Center-Shreveport, 1501 Kings Highway, Shreveport, LA 71130, USA. dmcgee@lsuhsc.edu
Alika E George
Elizabeth A Trainor
Katherine E Horton
Ellen Hildebrandt
Traci L Testerman

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The human gastric pathogen Helicobacter pylori steals host cholesterol, modifies it by glycosylation, and incorporates the glycosylated cholesterol onto its surface via a cholesterol glucosyltransferase, encoded by cgt. The impact of cholesterol on H. pylori antimicrobial resistance is unknown. H. pylori strain 26695 was cultured in Ham's F12 chemically defined medium in the presence or absence of cholesterol. The two cultures were subjected to overnight incubations with serial 2-fold dilutions of 12 antibiotics, six antifungals, and seven antimicrobial peptides (including LL-37 cathelicidin and human alpha and beta defensins). Of 25 agents tested, cholesterol-grown H. pylori cells were substantially more resistant (over 100-fold) to nine agents than were H. pylori cells grown without cholesterol. These nine agents included eight antibiotics and LL-37. H. pylori was susceptible to the antifungal drug pimaricin regardless of cholesterol presence in the culture medium. A cgt mutant retained cholesterol-dependent resistance to most antimicrobials but displayed increased susceptibility to colistin, suggesting an involvement of lipid A. Mutation of lpxE, encoding lipid A1-phosphatase, led to loss of cholesterol-dependent resistance to polymyxin B and colistin but not other antimicrobials tested. The cgt mutant was severely attenuated in gerbils, indicating that glycosylation is essential in vivo. These findings suggest that cholesterol plays a vital role in virulence and contributes to the intrinsic antibiotic resistance of H. pylori.

Indexed as

Anti-Bacterial AgentsAntifungal AgentsAntimicrobial Cationic PeptidesBacterial ProteinsBismuthCathelicidinsCell WallCholesterolDNA ReplicationDrug Resistance, BacterialFolic AcidHelicobacter pyloriHydrophobic and Hydrophilic InteractionsLipid AMonomeric GTP-Binding ProteinsOrganometallic CompoundsAnti-Bacterial AgentsAntifungal AgentsAntimicrobial Cationic PeptidesBacterial ProteinsBismuthbismuth subsalicylateCathelicidinsCgtA protein, bacteriaCholesterolFolic AcidLipid AMonomeric GTP-Binding ProteinsOrganometallic CompoundsPhosphoric Monoester HydrolasesProtein Synthesis InhibitorsSalicylates

Identifiers

PMID21464244
PMCPMC3101455

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.