Evidence map›Paper›PMID 31820077›Full record

ArticleLung2020

The Impact of Interleukin (IL)-33 Gene Polymorphisms and Environmental Factors on Risk of Asthma in the Iranian Population.

Mojdeh Matloubi, Maral Ranjbar, Mohammad-Ali Assarehzadegan, Morteza Fallahpour, Fatemeh Sadeghi, Saeed Soleyman-Jahi, Leila Janani

Abstract read
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In one paragraph

Article in Lung, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.5field-weighted citation impact, top 34% 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

7 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Targeting alarmins in asthma: From bench to clinic.The Journal of allergy and clinical immunology · 2025
    Review
  3. Review
  4. Journal of clinical medicine · 2023
    Article
  5. Review
  6. Review
  7. 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

7 authors at 2 institutions in 2 countries.

Mojdeh MatloubiDepartment of Medical Immunology, School of Medicine, Iran University of Medical Science, Hemmat Highway, Tehran, Iran.
Maral RanjbarDepartment of Medical Immunology, School of Medicine, Iran University of Medical Science, Hemmat Highway, Tehran, Iran.
Mohammad-Ali AssarehzadeganImmunology Research Center, Institute of Immunology and Infectious Diseases, Iran University of Medical Science, Tehran, Iran. assarehma@gmail.com.ORCID 0000-0002-0301-2862
Morteza FallahpourDepartment of Allergy and Clinical Immunology, Iran University of Medical Sciences, Tehran, Iran.
Fatemeh SadeghiDepartment of Medical Immunology, School of Medicine, Iran University of Medical Science, Hemmat Highway, Tehran, Iran.
Saeed Soleyman-JahiDigestive Diseases Research Core Center, Division of Gastroenterology, School of Medicine, Washington University, St. Louis, USA.
Leila JananiDepartment of Biostatistics, School of Public Health, Iran University of Medical Science, Tehran, Iran.
Iran University of Medical Sciences · IRWashington University in St. Louis · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAirway epithelial cells secrete Interleukin-33 in response to the different allergens. Several single nucleotide polymorphisms (SNP) of this cytokine have been reported to be involved in the development of asthma. We conducted this study to evaluate the impact of the two most common SNPs of the IL-33 gene (rs1342326 and rs3939286) and environmental factors on the susceptibility to asthma in the Iranian population. SUBJECTS AND

methodsIn this study, we enrolled 126 asthmatics patients and 300 age, sex-matched controls. Genotyping was performed by real-time PCR using the TaqMan SNP genotyping assay. Moreover, total serum IgE level, eosinophil count, and skin prick test were accomplished and complete history was taken from all the participants.

resultsThe frequencies of mutant genotypes in both SNPs were significantly higher in asthmatics than controls. C/C genotype of rs1342326 [OR (95% CI) 2.50 (1.33-4.69)] and A/A genotype of rs3939286 [OR (95% CI) 2.18 (1.05-4.52)] were associated with higher risk of asthma development. While A/C+C/C genotype of rs1342326 was more prevalent in mild asthma [OR (95% CI) 2.36 (1.14-4.89)], G/A+A/A genotype of rs3939286 was associated with increased risk of moderate and severe asthma [OR (95% CI) 2.53 (1.30-4.94)].

conclusionThis study revealed that both IL-33 SNPs were associated with an increased risk of asthma. The rs1342326 was associated with atopic, mild and adult-onset asthma and a higher level of eosinophils in peripheral blood. However, rs3939286 was more frequent in moderate and severe asthma. Moreover, rs3939286 was associated with non-atopic and childhood-onset asthma.

Indexed as

Gene-Environment InteractionAdultAge of OnsetAsthmaCase-Control StudiesEosinophiliaFemaleForced Expiratory VolumeGenetic Predisposition to DiseaseGenotypeHumansImmunoglobulin EInterleukin-33IranMaleMiddle AgedIL33 protein, humanImmunoglobulin EInterleukin-33AllergyAsthmaEnvironmental factorsInterleukin-33Single nucleotide polymorphism

Identifiers

PMID31820077
OpenAlexW2993579620

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.