Evidence map›Paper›PMID 29922273›Full record

ArticleFrontiers in immunology2018

Neutrophil Elastase Subverts the Immune Response by Cleaving Toll-Like Receptors and Cytokines in Pneumococcal Pneumonia.

Hisanori Domon, Kosuke Nagai, Tomoki Maekawa, Masataka Oda, Daisuke Yonezawa, Wataru Takeda, Takumi Hiyoshi, Hikaru Tamura, Masaya Yamaguchi, Shigetada Kawabata and 1 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
3.6field-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

45 citing papers in PubMed, 70 citations in OpenAlex.

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  6. Blocking HXAmBio · 2024
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  8. Blocking HXAbioRxiv : the preprint server for biology · 2024
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  13. On the path to predicting immune responses in the lung: Modeling the pulmonary innate immune system at the air-liquid interface (ALI).European journal of pharmaceutical sciences : official journal of the European Federation for Pharmaceutical Sciences · 2023
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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

11 authors at 3 institutions in 1 country.

Hisanori DomonDivision of Microbiology and Infectious Diseases, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan.
Kosuke NagaiDivision of Microbiology and Infectious Diseases, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan.
Tomoki MaekawaDivision of Microbiology and Infectious Diseases, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan.
Masataka OdaDepartment of Microbiology and Infection Control Sciences, Kyoto Pharmaceutical University, Kyoto, Japan.
Daisuke YonezawaDivision of Microbiology and Infectious Diseases, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan.
Wataru TakedaFaculty of Dentistry, Niigata University, Niigata, Japan.
Takumi HiyoshiDivision of Microbiology and Infectious Diseases, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan.
Hikaru TamuraDivision of Microbiology and Infectious Diseases, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan.
Masaya YamaguchiDepartment of Oral and Molecular Microbiology, Osaka University, Graduate School of Dentistry, Osaka, Japan.
Shigetada KawabataDepartment of Oral and Molecular Microbiology, Osaka University, Graduate School of Dentistry, Osaka, Japan.
Yutaka TeraoDivision of Microbiology and Infectious Diseases, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan.
Niigata University · JPOsaka University · JPKyoto Pharmaceutical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Excessive activation of neutrophils results in the release of neutrophil elastase (NE), which leads to lung injury in severe pneumonia. Previously, we demonstrated a novel immune subversion mechanism involving microbial exploitation of this NE ability, which eventually promotes disruption of the pulmonary epithelial barrier. In the present study, we investigated the effect of NE on host innate immune response. THP-1-derived macrophages were stimulated with heat-killed

Indexed as

AnimalsBronchoalveolar Lavage FluidCytokinesGlycineHumansImmunity, InnateLeukocyte ElastaseMaleMice, Inbred BALB CNF-kappa BPneumonia, PneumococcalSerine Proteinase InhibitorsStreptococcus pneumoniaeSulfonamidesTHP-1 CellsToll-Like ReceptorsCytokinesGlycineLeukocyte ElastaseNF-kappa BSerine Proteinase InhibitorssivelestatSulfonamidesToll-Like Receptorscytokinesinnate immune responseneutrophil elastasepneumoniaStreptococcus pneumoniaetoll-like receptor

Identifiers

PMID29922273
PMCPMC5996908
OpenAlexW2802300814

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.