Evidence map›Paper›PMID 24943899›Full record

ArticleClinical and experimental immunology2014

Functional relevance of NLRP3 inflammasome-mediated interleukin (IL)-1β during acute allergic airway inflammation.

M Ritter, K Straubinger, S Schmidt, D H Busch, S Hagner, H Garn, C Prazeres da Costa, L E Layland

Open access · bronzeAbstract read
In one paragraph

Article in Clinical and experimental immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.0field-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

34 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Canonical and non-canonical functions of NLRP3.Journal of advanced research · 2023
    Review
  8. Review
  9. IL-1Mediators of inflammation · 2023
    Review
  10. Article
  11. Article
  12. Article
  13. Neutrophils and Asthma.Diagnostics (Basel, Switzerland) · 2022
    Review
  14. Article
  15. NOD-like receptors in asthma.Frontiers in immunology · 2022
    Review
  16. Article
  17. FSTL1 aggravates OVA-induced inflammatory responses by activating the NLRP3/IL-1β signaling pathway in mice and macrophages.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2021
    Article
  18. Article
  19. Innate Immune Responses and Pulmonary Diseases.Advances in experimental medicine and biology · 2021
    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

8 authors at 3 institutions in 1 country.

M RitterInstitute of Medical Microbiology, Immunology and Parasitology (IMMIP), University Clinic Bonn, Bonn, Germany; Institute of Medical Microbiology, Immunology and Hygiene (MIH), Technische Universität München, Munich, Germany.
K Straubinger
S Schmidt
D H Busch
S Hagner
H Garn
C Prazeres da Costa
L E Layland
Institute of Medical Microbiology and Hygiene · DEPhilipps University of Marburg · DETechnical University of Munich · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Overall asthmatic symptoms can be controlled with diverse therapeutic agents. However, certain symptomatic individuals remain at risk for serious morbidity and mortality, which prompts the identification of novel therapeutic targets and treatment strategies. Thus, using an adjuvant-free T helper type 2 (Th2) murine model, we have deciphered the role of interleukin (IL)-1 signalling during allergic airway inflammation (AAI). Because functional IL-1β depends on inflammasome activation we first studied asthmatic manifestations in specific inflammasome-deficient [NACHT, LRR and PYD domains-containing protein 3 (NLRP3(-/-) ) and apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC(-/-) )] and IL-1 receptor type 1(-/-) (IL-1R1(-/-) ) mice on the BALB/c background. To verify the onset of disease we assessed cellular infiltration in the bronchial regions, lung pathology, airway hyperresponsiveness and ovalbumin (OVA)-specific immune responses. In the absence of NLRP3 inflammasome-mediated IL-1β release all symptoms of AAI were reduced, except OVA-specific immunoglobulin levels. To address whether manipulating IL-1 signalling reduced asthmatic development, we administered the IL-1R antagonist anakinra (Kineret®) during critical immunological time-points: sensitization or challenge. Amelioration of asthmatic symptoms was only observed when anakinra was administered during OVA challenge. Our findings indicate that blocking IL-1 signalling could be a potential complementary therapy for allergic airway inflammation.

Indexed as

Acute DiseaseAnimalsApoptosis Regulatory ProteinsCARD Signaling Adaptor ProteinsCarrier ProteinsCytokinesDisease Models, AnimalEosinophiliaFemaleGoblet CellsHyperplasiaInflammasomesInterleukin-1betaInterleukin 1 Receptor Antagonist ProteinMiceMice, KnockoutApoptosis Regulatory ProteinsCARD Signaling Adaptor ProteinsCarrier ProteinsCytokinesInflammasomesInterleukin-1betaInterleukin 1 Receptor Antagonist ProteinNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mouseOvalbuminPycard protein, mouseReceptors, Interleukin-1 Type IallergyanakinraIL-1 receptor antagonistIL-1βNLRP3-inflammasome

Identifiers

PMID24943899
PMCPMC4233370
OpenAlexW2103581795

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.