Evidence map›Paper›PMID 31590215›Full record

ReviewJournal of clinical medicine2019

Targeting NLRP3 Inflammasome Activation in Severe Asthma.

Efthymia Theofani, Maria Semitekolou, Ioannis Morianos, Konstantinos Samitas, Georgina Xanthou

Open access · goldAbstract readReview
In one paragraph

Review in Journal of clinical medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
3.9field-weighted citation impact, top 5% 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

62 citing papers in PubMed, 110 citations in OpenAlex.

  1. Review
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  7. [Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2026
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  10. NLRP3 inflammasome expression in pediatric asthma: sputum-based insights, inflammatory mechanisms, and targeted therapeutic strategies.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2025
    Review
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2 more citing papers are in PubMed but not listed here.

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

5 authors at 2 institutions in 1 country.

Efthymia TheofaniCellular Immunology Laboratory, Center for Basic Research, Biomedical Research Foundation of the Academy of Athens, 11527 Athens, Greece.
Maria SemitekolouCellular Immunology Laboratory, Center for Basic Research, Biomedical Research Foundation of the Academy of Athens, 11527 Athens, Greece.
Ioannis MorianosCellular Immunology Laboratory, Center for Basic Research, Biomedical Research Foundation of the Academy of Athens, 11527 Athens, Greece.
Konstantinos Samitas7th Respiratory Clinic and Asthma Center, 'Sotiria' Athens Chest Hospital, 11527 Athens, Greece.
Georgina XanthouCellular Immunology Laboratory, Center for Basic Research, Biomedical Research Foundation of the Academy of Athens, 11527 Athens, Greece. gxanthou@bioacademy.gr.ORCID 0000-0001-7944-2343
Biomedical Research Foundation of the Academy of Athens · GRSotiria General Hospital · GR

Funding

General Secretariat for Research and Technology 09-12-1074General Secretariat for Research and Technology 5035Hellenic Foundation for Research and Innovation 1030
6 · The paper itself

Abstract

Severe asthma (SA) is a chronic lung disease characterized by recurring symptoms of reversible airflow obstruction, airway hyper-responsiveness (AHR), and inflammation that is resistant to currently employed treatments. The nucleotide-binding oligomerization domain-like Receptor Family Pyrin Domain Containing 3 (NLRP3) inflammasome is an intracellular sensor that detects microbial motifs and endogenous danger signals and represents a key component of innate immune responses in the airways. Assembly of the NLRP3 inflammasome leads to caspase 1-dependent release of the pro-inflammatory cytokines IL-1β and IL-18 as well as pyroptosis. Accumulating evidence proposes that NLRP3 activation is critically involved in asthma pathogenesis. In fact, although NLRP3 facilitates the clearance of pathogens in the airways, persistent NLRP3 activation by inhaled irritants and/or innocuous environmental allergens can lead to overt pulmonary inflammation and exacerbation of asthma manifestations. Notably, administration of NLRP3 inhibitors in asthma models restrains AHR and pulmonary inflammation. Here, we provide an overview of the pathophysiology of SA, present molecular mechanisms underlying aberrant inflammatory responses in the airways, summarize recent studies pertinent to the biology and functions of NLRP3, and discuss the role of NLRP3 in the pathogenesis of asthma. Finally, we contemplate the potential of targeting NLRP3 as a novel therapeutic approach for the management of SA.

Indexed as

allergic airway inflammationIL-1βimmune regulationinnate immunityNLRP3severe asthma

Identifiers

PMID31590215
PMCPMC6833007
OpenAlexW2977578303

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.