Evidence map›Paper›PMID 26317436›Full record

ArticlePloS one2015

Serotype 1 and 8 Pneumococci Evade Sensing by Inflammasomes in Human Lung Tissue.

Diana Fatykhova, Anne Rabes, Christoph Machnik, Kunchur Guruprasad, Florence Pache, Johanna Berg, Mario Toennies, Torsten T Bauer, Paul Schneider, Maria Schimek and 9 more

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 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

27 citing papers in PubMed, 39 citations in OpenAlex.

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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

19 authors at 6 institutions in 3 countries.

Diana FatykhovaDepartment of Internal Medicine/Infectious Diseases and Pulmonary Medicine, Charité-Universitätsmedizin Berlin, Augustenburger Platz 1, 13353, Berlin, Germany.
Anne RabesDepartment of Internal Medicine/Infectious Diseases and Pulmonary Medicine, Charité-Universitätsmedizin Berlin, Augustenburger Platz 1, 13353, Berlin, Germany.
Christoph MachnikDepartment of Internal Medicine/Infectious Diseases and Pulmonary Medicine, Charité-Universitätsmedizin Berlin, Augustenburger Platz 1, 13353, Berlin, Germany.
Kunchur GuruprasadBioinformatics, Centre for Cellular and Molecular Biology, Hyderabad, Telangana, India.
Florence PacheDepartment of Internal Medicine/Infectious Diseases and Pulmonary Medicine, Charité-Universitätsmedizin Berlin, Augustenburger Platz 1, 13353, Berlin, Germany.
Johanna BergDepartment of Internal Medicine/Infectious Diseases and Pulmonary Medicine, Charité-Universitätsmedizin Berlin, Augustenburger Platz 1, 13353, Berlin, Germany.
Mario ToenniesLungenklinik Heckeshorn, HELIOS Klinikum Emil von Behring, Walterhöferstrasse 11, 14165, Berlin, Germany.
Torsten T BauerLungenklinik Heckeshorn, HELIOS Klinikum Emil von Behring, Walterhöferstrasse 11, 14165, Berlin, Germany.
Paul SchneiderDepartment for General and Thoracic Surgery, DRK Clinics, Drontheimer Strasse 39-40, 13359, Berlin, Germany.
Maria SchimekVivantes Klinikum Neukölln, Department for Thoracic Surgery, Berlin, Rudower Straße 48, 12351, Berlin, Germany.
Stephan EggelingVivantes Klinikum Neukölln, Department for Thoracic Surgery, Berlin, Rudower Straße 48, 12351, Berlin, Germany.
Timothy J MitchellInstitute of Microbiology and Infection, School of Infection and Immunity, University of Birmingham, Birmingham, B15-2TT, United Kingdom.
Andrea M MitchellInstitute of Microbiology and Infection, School of Infection and Immunity, University of Birmingham, Birmingham, B15-2TT, United Kingdom.
Rolf HilkerInstitute of Medical Microbiology, Justus-Liebig University Giessen, Schubertstrasse 81, D-35392, Giessen, Germany; Department of Bioinformatics and Systems Biology, Justus-Liebig University Giessen, Heinrich-Buff-Ring 58, D-35392, Giessen, Germany.
Torsten HainInstitute of Medical Microbiology, Justus-Liebig University Giessen, Schubertstrasse 81, D-35392, Giessen, Germany.
Norbert SuttorpDepartment of Internal Medicine/Infectious Diseases and Pulmonary Medicine, Charité-Universitätsmedizin Berlin, Augustenburger Platz 1, 13353, Berlin, Germany.
Stefan HippenstielDepartment of Internal Medicine/Infectious Diseases and Pulmonary Medicine, Charité-Universitätsmedizin Berlin, Augustenburger Platz 1, 13353, Berlin, Germany.
Andreas C HockeDepartment of Internal Medicine/Infectious Diseases and Pulmonary Medicine, Charité-Universitätsmedizin Berlin, Augustenburger Platz 1, 13353, Berlin, Germany.
Bastian OpitzDepartment of Internal Medicine/Infectious Diseases and Pulmonary Medicine, Charité-Universitätsmedizin Berlin, Augustenburger Platz 1, 13353, Berlin, Germany.
Charité - Universitätsmedizin Berlin · DEHelios Klinikum Emil von Behring · DEUniversity of Birmingham · GBUniversity of Giessen · DEVivantes Klinikum · DECentre for Cellular and Molecular Biology · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Streptococcus pneumoniae is a major cause of pneumonia, sepsis and meningitis. The pore-forming toxin pneumolysin is a key virulence factor of S. pneumoniae, which can be sensed by the NLRP3 inflammasome. Among the over 90 serotypes, serotype 1 pneumococci (particularly MLST306) have emerged across the globe as a major cause of invasive disease. The cause for its particularity is, however, incompletely understood. We therefore examined pneumococcal infection in human cells and a human lung organ culture system mimicking infection of the lower respiratory tract. We demonstrate that different pneumococcal serotypes differentially activate inflammasome-dependent IL-1β production in human lung tissue and cells. Whereas serotype 2, 3, 6B, 9N pneumococci expressing fully haemolytic pneumolysins activate NLRP3 inflammasome-dependent responses, serotype 1 and 8 strains expressing non-haemolytic toxins are poor activators of IL-1β production. Accordingly, purified haemolytic pneumolysin but not serotype 1-associated non-haemolytic toxin activates strong IL-1β production in human lungs. Our data suggest that the evasion of inflammasome-dependent innate immune responses by serotype 1 pneumococci might contribute to their ability to cause invasive diseases in humans.

Indexed as

Bacterial ProteinsCaspase 1HemolysisHumansInflammasomesInterleukin-1betaLungSpecies SpecificityStreptococcus pneumoniaeStreptolysinsBacterial ProteinsCaspase 1InflammasomesInterleukin-1betaplY protein, Streptococcus pneumoniaeStreptolysins

Identifiers

PMID26317436
PMCPMC4552725
OpenAlexW1909210767

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.