Evidence map›Paper›PMID 26641098›Full record

ArticlePloS one2015

Phosphoethanolamine Modification of Neisseria gonorrhoeae Lipid A Reduces Autophagy Flux in Macrophages.

Susu M Zughaier, Justin L Kandler, Jacqueline T Balthazar, William M Shafer

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

18 citing papers in PubMed, 26 citations in OpenAlex.

  1. Lipid A modification of colistin-resistantInfection and immunity · 2024
    Article
  2. Review
  3. Mechanisms of host manipulation byFrontiers in microbiology · 2023
    Review
  4. Article
  5. Article
  6. Article
  7. Anti-Virulence Therapeutic Approaches forAntibiotics (Basel, Switzerland) · 2021
    Review
  8. Article
  9. Identification of aPathogens (Basel, Switzerland) · 2020
    Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Macrophage-Frontiers in immunology · 2018
    Review
  15. Review
  16. Article
  17. Analysis of novel meningococcal vaccine formulations.Human vaccines & immunotherapeutics · 2017
    Article
  18. Structure-Activity Relationship ofFrontiers in immunology · 2017
    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 2 institutions in 1 country.

Susu M ZughaierLaboratory of Bacterial Pathogenesis, Department of Veterans Affairs Medical Center Decatur, Atlanta, Georgia, United States of America.
Justin L KandlerDepartment of Microbiology and Immunology, Emory University School of Medicine, Atlanta, Georgia, United States of America.
Jacqueline T BalthazarDepartment of Microbiology and Immunology, Emory University School of Medicine, Atlanta, Georgia, United States of America.
William M ShaferLaboratory of Bacterial Pathogenesis, Department of Veterans Affairs Medical Center Decatur, Atlanta, Georgia, United States of America.
Emory University · USVeterans Health Administration · US

Funding

The Atlantic Coast Sexually Transmitted Infection Cooperative Research Center (ACU19AI113170 · NIAID · HENRY M. JACKSON FDN FOR THE ADV MIL/MED · PI JERSE, ANN E. · 2014 to 2018
$6.9M
Gonococcal Mechanisms to Evade Host DefensesI01BX000112 · VA · VETERANS HEALTH ADMINISTRATION · PI SHAFER, WILLIAM MAURICE · 2009 to 2017
–
BLRD VA I01 BX000112NIAID NIH HHS 1U19AI113170-01NIAID NIH HHS U19 AI113170
6 · The paper itself

Abstract

Autophagy, an ancient homeostasis mechanism for macromolecule degradation, performs an important role in host defense by facilitating pathogen elimination. To counteract this host defense strategy, bacterial pathogens have evolved a variety of mechanisms to avoid or otherwise dysregulate autophagy by phagocytic cells so as to enhance their survival during infection. Neisseria gonorrhoeae is a strictly human pathogen that causes the sexually transmitted infection, gonorrhea. Phosphoethanolamine (PEA) addition to the 4' position of the lipid A (PEA-lipid A) moiety of the lipooligosaccharide (LOS) produced by gonococci performs a critical role in this pathogen's ability to evade innate defenses by conferring decreased susceptibility to cationic antimicrobial (or host-defense) peptides, complement-mediated killing by human serum and intraleukocytic killing by human neutrophils compared to strains lacking this PEA decoration. Heretofore, however, it was not known if gonococci can evade autophagy and if so, whether PEA-lipid A contributes to this ability. Accordingly, by using murine macrophages and human macrophage-like phagocytic cell lines we investigated if PEA decoration of gonococcal lipid A modulates autophagy formation. We report that infection with PEA-lipid A-producing gonococci significantly reduced autophagy flux in murine and human macrophages and enhanced gonococcal survival during their association with macrophages compared to a PEA-deficient lipid A mutant. Our results provide further evidence that PEA-lipid A produced by gonococci is a critical component in the ability of this human pathogen to evade host defenses.

Indexed as

EthanolaminesAnimalsAutophagyCell LineChemokinesDisaccharidesHost-Pathogen InteractionsHumansLipid AMacrophagesMiceNeisseria gonorrhoeaePhagosomesSugar PhosphatesChemokinesDisaccharideseritoranEthanolaminesLipid AphosphorylethanolamineSugar Phosphates

Identifiers

PMID26641098
PMCPMC4671640
OpenAlexW2288763580

What OpenQuestion holds

Textmetadata
LicenceCC0
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.