Evidence map›Paper›PMID 27430279›Full record

ArticleBMC microbiology2016

Clinical Streptococcus pneumoniae isolates induce differing CXCL8 responses from human nasopharyngeal epithelial cells which are reduced by liposomes.

Denja Baumgartner, Suzanne Aebi, Denis Grandgirard, Stephen L Leib, Annette Draeger, Eduard Babiychuk, Lucy J Hathaway

Open access · goldAbstract read
In one paragraph

Article in BMC microbiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 13% 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

10 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.

  1. Liposomes from red betel (Open veterinary journal · 2025
    Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Frontiers in microbiology · 2020
    Article
  8. Article
  9. Article
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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

7 authors at 1 institution in 1 country.

Denja BaumgartnerFaculty of Medicine, Institute for Infectious Diseases, University of Bern, Friedbühlstrasse 51, Bern, CH-3001, Switzerland.
Suzanne AebiFaculty of Medicine, Institute for Infectious Diseases, University of Bern, Friedbühlstrasse 51, Bern, CH-3001, Switzerland.
Denis GrandgirardFaculty of Medicine, Institute for Infectious Diseases, University of Bern, Friedbühlstrasse 51, Bern, CH-3001, Switzerland.
Stephen L LeibFaculty of Medicine, Institute for Infectious Diseases, University of Bern, Friedbühlstrasse 51, Bern, CH-3001, Switzerland.
Annette DraegerFaculty of Medicine, Institute of Anatomy, University of Bern, Baltzerstrasse 2, Bern, CH-3012, Switzerland.
Eduard BabiychukFaculty of Medicine, Institute of Anatomy, University of Bern, Baltzerstrasse 2, Bern, CH-3012, Switzerland.
Lucy J HathawayFaculty of Medicine, Institute for Infectious Diseases, University of Bern, Friedbühlstrasse 51, Bern, CH-3001, Switzerland. lucy.hathaway@ifik.unibe.ch.
University of Bern · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundStreptococcus pneumoniae causes several human diseases, including pneumonia and meningitis, in which pathology is associated with an excessive inflammatory response. A major inducer of this response is the cholesterol dependent pneumococcal toxin, pneumolysin. Here, we measured the amount of inflammatory cytokine CXCL8 (interleukin (IL)-8) by ELISA released by human nasopharyngeal epithelial (Detroit 562) cells as inflammatory response to a 24 h exposure to different pneumococcal strains.

resultsWe found pneumolysin to be the major factor influencing the CXCL8 response. Cholesterol and sphingomyelin-containing liposomes designed to sequester pneumolysin were highly effective at reducing CXCL8 levels from epithelial cells exposed to different clinical pneumococcal isolates. These liposomes also reduced CXCL8 response from epithelial cells exposed to pneumolysin knock-out mutants of S. pneumoniae indicating that they also reduce the CXCL8-inducing effect of an unidentified pneumococcal virulence factor, in addition to pneumolysin.

conclusionThe results indicate the potential of liposomes in attenuating excessive inflammation as a future adjunctive treatment of pneumococcal diseases.

Indexed as

Bacterial CapsulesBacterial ProteinsCell LineCells, CulturedCholesterolCytokinesEpithelial CellsHumansInterleukin-8LiposomesMutationNasopharynxSphingomyelinsStreptococcus pneumoniaeStreptolysinsBacterial ProteinsCholesterolCXCL8 protein, humanCytokinesInterleukin-8LiposomesplY protein, Streptococcus pneumoniaeSphingomyelinsStreptolysinsCapsuleCXCL8LiposomesPneumolysinStreptococcus pneumoniae

Identifiers

PMID27430279
PMCPMC4950757
OpenAlexW2500156413

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.