Evidence map›Paper›PMID 27956597›Full record

ArticleInfection and immunity2017

Tet38 Efflux Pump Affects Staphylococcus aureus Internalization by Epithelial Cells through Interaction with CD36 and Contributes to Bacterial Escape from Acidic and Nonacidic Phagolysosomes.

Q C Truong-Bolduc, N S Khan, J M Vyas, D C Hooper

Open access · bronzeAbstract read
In one paragraph

Article in Infection and immunity, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

20 citing papers in PubMed, 28 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Decoding the evolutionary history of ST30Frontiers in microbiology · 2025
    Article
  5. Microglial activation states and their implications for Alzheimer's Disease.The journal of prevention of Alzheimer's disease · 2025
    Review
  6. Role of bacterial multidrug efflux pumps during infection.World journal of microbiology & biotechnology · 2024
    Review
  7. Antimicrobial agents and chemotherapy · 2024
    Article
  8. NorA efflux pump mediatesAntimicrobial agents and chemotherapy · 2024
    Article
  9. AIMS microbiology · 2023
    Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. Frontiers in cellular and infection microbiology · 2017
    Review
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 1 institution in 1 country.

Q C Truong-BolducDivision of Infectious Diseases, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA.
N S KhanDivision of Infectious Diseases, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA.
J M VyasDivision of Infectious Diseases, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA.ORCID http://orcid.org/0000-0002-9985-9565
D C HooperDivision of Infectious Diseases, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA dhooper@mgh.harvard.edu.
Harvard University · US

Funding

Technical Mother Machine CoreP01AI083214 · NIAID · SCHEPENS EYE RESEARCH INSTITUTE · PI Michael S Gilmore · 2009 to 2026
$39.4M
Quinolone and multidrug resistance in Staphylococcus aureusR37AI023988 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI HOOPER, DAVID C · 2008 to 2017
$4.1M
NIAID NIH HHS P01 AI083214NIAID NIH HHS R37 AI023988
6 · The paper itself

Abstract

We previously reported that the Tet38 efflux pump is involved in internalization of Staphylococcus aureus by A549 lung epithelial cells. A lack of tet38 reduced bacterial uptake by A549 cells to 36% of that of the parental strain RN6390. Using invasion assays coupled with confocal microscopy imaging, we studied the host cell receptor(s) responsible for bacterial uptake via interaction with Tet38. We also assessed the ability of S. aureus to survive following alkalinization of the phagolysosomes by chloroquine. Antibody to the scavenger receptor CD36 reduced the internalization of S. aureus RN6390 by A549 cells, but the dependence on CD36 was reduced in QT7 tet38, suggesting that an interaction between Tet38 and CD36 contributed to S. aureus internalization. Following fusion of the S. aureus-associated endosomes with lysosomes, alkalinization of the acidic environment with chloroquine led to a rapid increase in the number of S. aureus RN6390 bacteria in the cytosol, followed by a decrease shortly thereafter. This effect of chloroquine was not seen in the absence of intact Tet38 in mutant QT7. These data taken together suggest that Tet38 plays a role both in bacterial internalization via interaction with CD36 and in bacterial escape from the phagolysosomes.

Indexed as

Host-Pathogen InteractionsAntibodies, MonoclonalBacterial ProteinsCD36 AntigensCell LineChloroquineEpithelial CellsHumansMicrobial ViabilityPhagosomesProtein BindingStaphylococcal InfectionsStaphylococcus aureusToll-Like Receptor 2Antibodies, MonoclonalBacterial ProteinsCD36 AntigensChloroquineToll-Like Receptor 2CD36endosomesinternalizationS. aureussurvival

Identifiers

PMID27956597
PMCPMC5278174
OpenAlexW2565933219

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.