Evidence map›Paper›PMID 20974830›Full record

ArticleInfection and immunity2011

Role of the HefC efflux pump in Helicobacter pylori cholesterol-dependent resistance to ceragenins and bile salts.

Elizabeth A Trainor, Katherine E Horton, Paul B Savage, Traci L Testerman, David J McGee

Open access · bronzeAbstract read
In one paragraph

Article in Infection and immunity, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.0field-weighted citation impact, top 9% of its field
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

27 citing papers in PubMed, 50 citations in OpenAlex.

  1. Review
  2. 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
    Article
  3. International journal of molecular sciences · 2024
    Review
  4. Article
  5. Article
  6. Global Antimicrobial Resistance Gene Study ofAntibiotics (Basel, Switzerland) · 2023
    Article
  7. Microbiology (Reading, England) · 2023
    Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. AFrontiers in cellular and infection microbiology · 2017
    Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article
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

5 authors at 2 institutions in 1 country.

Elizabeth A TrainorDepartment of Microbiology and Immunology, Louisiana State University Health Sciences Center-Shreveport, MSB 2-225, 1501 Kings Highway, Shreveport, LA 71130, USA.
Katherine E Horton
Paul B Savage
Traci L Testerman
David J McGee
Louisiana State University Health Sciences Center Shreveport · USBrigham Young University · US

Funding

H.pylori arginase modulation of ulcers and cancerR01CA101931 · NCI · UNIVERSITY OF SOUTH ALABAMA · PI MCGEE, DAVID J · 2003 to 2007
$1.6M
NCI NIH HHS R01 CA101931
6 · The paper itself

Abstract

The human gastric pathogen Helicobacter pylori modifies host cholesterol via glycosylation and incorporates the glycosylated cholesterol into its membrane; however, the benefits of cholesterol to H. pylori are largely unknown. We speculated that cholesterol in the H. pylori membrane might alter the susceptibility of these organisms to membrane-disrupting antibacterial compounds. To test this hypothesis, H. pylori strains were cultured in Ham's F-12 chemically defined medium in the presence or absence of cholesterol. The two cultures were subjected to overnight incubations with serial 2-fold dilutions of 10 bile salts and four ceragenins, which are novel bile salt derivatives that mimic membrane-disrupting activity of antimicrobial peptides. H. pylori cultured with cholesterol was substantially more resistant to seven of the bile salts and three ceragenins than H. pylori cultured without cholesterol. In most cases, these cholesterol-dependent differences ranged from 2 to 7 orders of magnitude; this magnitude depended on concentration of the agent. Cholesterol is modified by glycosylation using Cgt, a cholesteryl glycosyltransferase. Surprisingly, a cgt knockout strain still maintained cholesterol-dependent resistance to bile salts and ceragenins, indicating that cholesterol modification was not involved in resistance. We then tested whether three putative, paralogous inner membrane efflux pumps, HefC, HefF, or HefI, played a role. While HefF and HefI appeared unimportant, HefC was shown to play a critical role in the resistance to bile salts and ceragenins by multiple methods in multiple strain backgrounds. Thus, both cholesterol and the putative bile salt efflux pump HefC play important roles in H. pylori resistance to bile salts and ceragenins.

Indexed as

Bacterial ProteinsBile Acids and SaltsCarrier ProteinsCholesterolDrug Resistance, BacterialGene Expression Regulation, BacterialHelicobacter pyloriMolecular StructureMutationSteroidsBacterial ProteinsBile Acids and SaltsCarrier ProteinsCholesterolSteroids

Identifiers

PMID20974830
PMCPMC3019907
OpenAlexW2162165243

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.