Evidence map›Paper›PMID 20659292›Full record

ArticleMolecular microbiology2010

Removal of the outer Kdo from Helicobacter pylori lipopolysaccharide and its impact on the bacterial surface.

Christopher M Stead, Jinshi Zhao, Christian R H Raetz, M Stephen Trent

Open access · greenAbstract read
In one paragraph

Article in Molecular microbiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
5.3field-weighted citation impact, top 5% 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

33 citing papers in PubMed, 56 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Single-step genome engineering in the bee gut symbiontbioRxiv : the preprint server for biology · 2023
    Article
  6. A Tripartite Efflux System Affects Flagellum Stability inInternational journal of molecular sciences · 2022
    Article
  7. Article
  8. Article
  9. Article
  10. A Newly Discovered Drug Resistance GeneInfection and drug resistance · 2019
    Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Disruption of lipid homeostasis in the Gram-negative cell envelope activates a novel cell death pathway.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  17. Review
  18. Article
  19. Kdo2 -lipid A: structural diversity and impact on immunopharmacology.Biological reviews of the Cambridge Philosophical Society · 2015
    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

4 authors at 3 institutions in 1 country.

Christopher M SteadDepartment of Biochemistry and Molecular Biology, Medical College of Georgia, Augusta, GA 30912, USA.
Jinshi Zhao
Christian R H Raetz
M Stephen Trent
Duke Medical Center · USAugusta University · USThe University of Texas at Austin · US

Funding

MODIFICATION OF HELICOBACTER PYLORI LIPOPOLYSACCHARIDESR01AI064184 · NIAID · UNIVERSITY OF TEXAS AT AUSTIN · PI TRENT, MICHAEL STEPHEN · 2006 to 2015
$3.4M
The Outer Surface of Vibrio CholeraeR01AI076322 · NIAID · UNIVERSITY OF TEXAS AT AUSTIN · PI TRENT, MICHAEL STEPHEN · 2008 to 2017
$3.2M
LIPID A MODIFICATION SYSTEMS IN GRAM-NEGATIVE BACTERIAR37GM051796 · NIGMS · DUKE UNIVERSITY · PI RAETZ, CHRISTIAN R · 1999 to 2008
$3.0M
Lipid A Modification Systems in Gram-Negative BacteriaR01GM051796 · NIGMS · DUKE UNIVERSITY · PI ZHOU, PEI · 1995 to 2012
$1.5M
The Outer Surface of Vibrio choleraeR56AI076322 · NIAID · UNIVERSITY OF TEXAS AT AUSTIN · PI TRENT, MICHAEL STEPHEN · 2013 to 2013
$384k
NIAID NIH HHS AI064184NIAID NIH HHS AI76322NIAID NIH HHS R01 AI064184NIAID NIH HHS R01 AI076322NIAID NIH HHS R56 AI076322NIGMS NIH HHS GM51796NIGMS NIH HHS R01 GM051796NIGMS NIH HHS R37 GM051796
6 · The paper itself

Abstract

Helicobacter pylori produces a unique surface lipopolysaccharide (LPS) characterized by strikingly low endotoxicity that is thought to aid the organism in evading the host immune response. This reduction in endotoxicity is predicted to arise from the modification of the Kdo-lipid A domain of Helicobacter LPS by a series of membrane bound enzymes including a Kdo (3-deoxy-d-manno-octulosonic acid) hydrolase responsible for the modification of the core oligosaccharide. Here, we report that Kdo hydrolase activity is dependent upon a putative two-protein complex composed of proteins Hp0579 and Hp0580. Inactivation of Kdo hydrolase activity produced two phenotypes associated with cationic antimicrobial peptide resistance and O-antigen expression. Kdo hydrolase mutants were highly sensitive to polymyxin B, which could be attributed to a defect in downstream modifications to the lipid A 4'-phosphate group. Production of a fully extended O-antigen was also diminished in a Kdo hydrolase mutant, with a consequent increase in core-lipid A. Finally, expression of O-antigen Lewis X and Y epitopes, known to mimic glycoconjugates found on human tissues, was also affected. Taken together, we have demonstrated that loss of Kdo hydrolase activity affects all three domains of H. pylori LPS, thus highlighting its role in the maintenance of the bacterial surface.

Indexed as

Anti-Bacterial AgentsAntimicrobial Cationic PeptidesBacterial ProteinsGene ExpressionGene Knockout TechniquesHelicobacter pyloriHumansHydrolasesLewis Blood Group AntigensLewis X AntigenLipopolysaccharidesO AntigensPolymyxin BSugar Acids2-keto-3-deoxyoctonateAnti-Bacterial AgentsAntimicrobial Cationic PeptidesBacterial ProteinsHydrolasesLewis Blood Group AntigensLewis X AntigenLewis Y antigenlipopolysaccharide, Helicobacter pyloriLipopolysaccharidesO AntigensPolymyxin BSugar Acids

Identifiers

PMID20659292
PMCPMC2978256
OpenAlexW1568638001

What OpenQuestion holds

Textmetadata
LicenceTDM
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.