Evidence map›Paper›PMID 36947565›Full record

ArticlePloS one2023

Single nucleotide variants in the IL33 and IL1RL1 (ST2) genes are associated with periodontitis and with Aggregatibacter actinomycetemcomitans in the dental plaque biofilm: A putative role in understanding the host immune response in periodontitis.

Soraya C Trindade, Mabel P P Lopes, Tatiane T M C Oliveira, Milca J Silva, Gerson A Queiroz, Talita S Jesus, Ellen K N Santos, Paulo C Carvalho-Filho, Michelle M L Falcão, Patrícia M Miranda and 5 more

Open access · goldFull text read
In one paragraph

Article in PloS one, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.9field-weighted citation impact, top 28% 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

2 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. The Influence of Genetic Polymorphisms ofInternational journal of dentistry · 2025
    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

15 authors at 3 institutions in 2 countries.

Soraya C TrindadePostgraduate Program in Immunology, Federal University of Bahia, Salvador, Bahia, Brazil.ORCID 0000-0001-7125-9114
Mabel P P LopesPostgraduate Program in Immunology, Federal University of Bahia, Salvador, Bahia, Brazil.
Tatiane T M C OliveiraPostgraduate Program in Immunology, Federal University of Bahia, Salvador, Bahia, Brazil.
Milca J SilvaPostgraduate Program in Immunology, Federal University of Bahia, Salvador, Bahia, Brazil.
Gerson A QueirozPostgraduate Program in Immunology, Federal University of Bahia, Salvador, Bahia, Brazil.
Talita S JesusPostgraduate Program in Immunology, Federal University of Bahia, Salvador, Bahia, Brazil.ORCID 0000-0003-1572-6472
Ellen K N SantosPostgraduate Program in Immunology, Federal University of Bahia, Salvador, Bahia, Brazil.ORCID 0000-0001-5633-8260
Paulo C Carvalho-FilhoPostgraduate Program in Immunology, Federal University of Bahia, Salvador, Bahia, Brazil.
Michelle M L FalcãoPostgraduate Program in Immunology, Federal University of Bahia, Salvador, Bahia, Brazil.ORCID 0000-0002-0929-2324
Patrícia M MirandaPostgraduate Program in Immunology, Federal University of Bahia, Salvador, Bahia, Brazil.
Rebeca P B SantosPostgraduate Program in Immunology, Federal University of Bahia, Salvador, Bahia, Brazil.
Camila A FigueiredoPostgraduate Program in Immunology, Federal University of Bahia, Salvador, Bahia, Brazil.
Álvaro A CruzPostgraduate Program in Health Sciences, Federal University of Bahia, Salvador, Bahia, Brazil.
Gregory J SeymourOral Health Centre, The University of Queensland, Herston, Queensland, Australia.
Isaac S Gomes-FilhoDepartment of Health, Feira de Santana State University, Feira de Santana, Bahia, Brazil.ORCID 0000-0002-4270-8491
Universidade Federal da Bahia · BRThe University of Queensland · AUUniversidade Estadual de Feira de Santana · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Interleukin (IL)-33 is important in several inflammatory diseases and its cellular receptor is the Interleukin 1 receptor-like 1 (IL1RL1), also called suppression of tumorigenicity 2 ligand (ST2L). This study investigated associations between single nucleotide variants (SNVs) in the IL33 gene and in the IL1RL1 (ST2) gene with periodontitis. Additionally, aimed to determine the role of Aggregatibacter actinomycetemcomitans (Aa) relative amount in the subgingival biofilm in these associations. A cross-sectional study was carried out with 506 individuals that answered a structured questionnaire used to collect their health status, socioeconomic-demographic, and behavioral characteristics. Periodontal examination was performed to determine the presence and severity of periodontitis, and subgingival biofilm samples were collected to quantify the relative amount of Aa by real time polymerase chain reaction. Human genomic DNA was extracted from whole blood cells and SNV genotyping was performed. Logistic regression estimated the association measurements, odds ratio (OR), and 95% confidence interval (95%CI), between the IL33 and ST2 genes with periodontitis, and subgroup analyses assessed the relative amount of Aa in these associations. 23% of individuals had periodontitis. Adjusted measurements showed a statistically significant inverse association between two SNVs of the ST2; rs148548829 (C allele) and rs10206753 (G allele). These two alleles together with a third SNV, the rs11693204 (A allele), were inversely associated with moderate periodontitis. One SNV of the IL33 gene also showed a statistically significant inverse association with moderate periodontitis. Nine SNVs of the ST2 gene were inversely associated with the relative amount of Aa. In the high Aa subgroup, there was a direct association between 11 SNVs of the ST2 gene and moderate periodontitis and two SNVs of the ST2 gene and severe periodontitis, and eight SNVs of the ST2 gene and periodontitis. These exploratory findings of genetic variants in IL-33/ST2 axis support the concept that the different tissue responses among individuals with periodontitis may be modulated by the host's genetics, influencing the physiopathology of the disease.

Indexed as

Dental PlaqueInterleukin-1 Receptor-Like 1 ProteinInterleukin-33PeriodontitisAggregatibacter actinomycetemcomitansBiofilmsCross-Sectional StudiesHumansImmunityNucleotidesPolymorphism, Single NucleotideIL1RL1 protein, humanIL33 protein, humanInterleukin-1 Receptor-Like 1 ProteinInterleukin-33Nucleotides

Identifiers

PMID36947565
PMCPMC10032506
OpenAlexW4353018911

What OpenQuestion holds

Textfull text, public
LicenceCC BY
measurements read66
identifiers read7
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.