Evidence map›Paper›PMID 28601872›Full record

ArticleJournal of innate immunity2017

IL-37 Causes Excessive Inflammation and Tissue Damage in Murine Pneumococcal Pneumonia.

Anja E Schauer, Tilman E Klassert, Carolin von Lachner, Diana Riebold, Anne Schneeweiß, Magdalena Stock, Mario M Müller, Sven Hammerschmidt, Philip Bufler, Ulrike Seifert and 6 more

Open access · goldAbstract read
In one paragraph

Article in Journal of innate immunity, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

15 citing papers in PubMed, 30 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

16 authors at 8 institutions in 4 countries.

Anja E SchauerSeptomics Research Center, Jena University Hospital, Jena, Germany.
Tilman E Klassert
Carolin von Lachner
Diana Riebold
Anne Schneeweiß
Magdalena Stock
Mario M Müller
Sven Hammerschmidt
Philip Bufler
Ulrike Seifert
Kristina Dietert
Charles A Dinarello
Marcel F Nold
Achim D Gruber
Claudia A Nold-Petry
Hortense Slevogt
Jena University Hospital · DEFreie Universität Berlin · DEHudson Institute of Medical Research · AUFriedrich-Loeffler-Institut · DEInfectoGnostics Research Campus Jena · DEPediatrics and Genetics · USRadboud University Nijmegen · NLUniversität Greifswald · DE

Funding

Yeast-based HTS Assay Technologies for ProteasesR01AI015614 · NIAID · UNIVERSITY OF COLORADO DENVER · PI DINARELLO, CHARLES ANTHONY · 1985 to 2025
$8.5M
Pathogenesis of Fever in ManR56AI015614 · NIAID · UNIVERSITY OF COLORADO DENVER · PI DINARELLO, CHARLES ANTHONY · 2016 to 2016
$311k
NIAID NIH HHS R01 AI015614NIAID NIH HHS R56 AI015614
6 · The paper itself

Abstract

Streptococcus pneumoniae infections can lead to severe complications with excessive immune activation and tissue damage. Interleukin-37 (IL-37) has gained importance as a suppressor of innate and acquired immunity, and its effects have been therapeutic as they prevent tissue damage in autoimmune and inflammatory diseases. By using RAW macrophages, stably transfected with human IL-37, we showed a 70% decrease in the cytokine levels of IL-6, TNF-α, and IL-1β, and a 2.2-fold reduction of the intracellular killing capacity of internalized pneumococci in response to pneumococcal infection. In a murine model of infection with S. pneumoniae, using mice transgenic for human IL-37b (IL-37tg), we observed an initial decrease in cytokine expression of IL-6, TNF-α, and IL-1β in the lungs, followed by a late-phase enhancement of pneumococcal burden and subsequent increase of proinflammatory cytokine levels. Additionally, a marked increase in recruitment of alveolar macrophages and neutrophils was noted, while TRAIL mRNA was reduced 3-fold in lungs of IL-37tg mice, resulting in necrotizing pneumonia with augmented death of infiltrating neutrophils, enhanced bacteremic spread, and increased mortality. In conclusion, we have identified that IL-37 modulates several core components of a successful inflammatory response to pneumococcal pneumonia, which lead to increased inflammation, tissue damage, and mortality.

Indexed as

AnimalsBacterial LoadBacteriolysisCytokinesDisease Models, AnimalHumansInflammation MediatorsInterleukin-1LungMacrophages, AlveolarMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicNeutrophilsPneumonia, PneumococcalCytokinesIL37 protein, humanInflammation MediatorsInterleukin-1TNF-Related Apoptosis-Inducing LigandAntibacterial host defenseImmunosuppressionInflammationInterleukin-37Pneumococcal pneumoniaStreptococcus pneumoniae

Identifiers

PMID28601872
PMCPMC6738772
OpenAlexW2622128062

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.