Evidence map›Paper›PMID 27732665›Full record

ArticlePLoS pathogens2016

Single Cell Bottlenecks in the Pathogenesis of Streptococcus pneumoniae.

Masamitsu Kono, M Ammar Zafar, Marisol Zuniga, Aoife M Roche, Shigeto Hamaguchi, Jeffrey N Weiser

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
5.7field-weighted citation impact, top 4% 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

55 citing papers in PubMed, 85 citations in OpenAlex.

  1. Article
  2. Bacterial and host factors affecting acquisition ofbioRxiv : the preprint server for biology · 2026
    Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Mechanisms of bacterial host-to-host transmission.Microbiology and molecular biology reviews : MMBR · 2025
    Review
  8. Article
  9. Review
  10. Bacteria and host: what does this mean for sepsis bottleneck?World journal of emergency medicine · 2025
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  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

6 authors at 3 institutions in 2 countries.

Masamitsu KonoDepartment of Microbiology, New York University, New York, New York, United States of America.ORCID http://orcid.org/0000-0002-7896-4892
M Ammar ZafarDepartment of Microbiology, New York University, New York, New York, United States of America.
Marisol ZunigaDepartment of Microbiology, New York University, New York, New York, United States of America.
Aoife M RocheDepartment of Microbiology, University of Pennsylvania, Philadelphia, Pennsylvania, United States of America.
Shigeto HamaguchiDepartment of Microbiology, New York University, New York, New York, United States of America.
Jeffrey N WeiserDepartment of Microbiology, New York University, New York, New York, United States of America.
New York University · USUniversity of Pennsylvania · USWakayama Medical University · JP

Funding

ROLE OF OPACITY VARIATION IN PNEUMOCOCCAL PATHOGENESISR01AI038446 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI WEISER, JEFFREY NEAL · 1996 to 2019
$7.4M
Mechanisms of Pneumococcal Persistence During CarriageR37AI038446 · NIAID · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI Jeffrey Neal Weiser · 2020 to 2026
$3.8M
Early Events in Pneumococcal ColonizationR01AI105168 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI WEISER, JEFFREY NEAL · 2014 to 2018
$2.1M
NIAID NIH HHS R01 AI038446NIAID NIH HHS R01 AI105168NIAID NIH HHS R37 AI038446
6 · The paper itself

Abstract

Herein, we studied a virulent isolate of the leading bacterial pathogen Streptococcus pneumoniae in an infant mouse model of colonization, disease and transmission, both with and without influenza A (IAV) co-infection. To identify vulnerable points in the multiple steps involved in pneumococcal pathogenesis, this model was utilized for a comprehensive analysis of population bottlenecks. Our findings reveal that in the setting of IAV co-infection the organism must pass through single cell bottlenecks during bloodstream invasion from the nasopharynx within the host and in transmission between hosts. Passage through these bottlenecks was not associated with genetic adaptation by the pathogen. The bottleneck in transmission occurred between bacterial exit from one host and establishment in another explaining why the number of shed organisms in secretions is critical to overcoming it. These observations demonstrate how viral infection, and TLR-dependent innate immune responses it stimulates and that are required to control it, drive bacterial contagion.

Indexed as

CoinfectionAnimalsDisease Models, AnimalFlow CytometryInfluenza A virusMiceMice, Inbred C57BLOrthomyxoviridae InfectionsPneumococcal InfectionsStreptococcus pneumoniae

Identifiers

PMID27732665
PMCPMC5061371
OpenAlexW2531115075

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.