Evidence map›Paper›PMID 38360807›Full record

ArticleAllergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology2024

Immune endotyping and gene expression profile of patients with chronic rhinosinusitis with nasal polyps in the aspirin-exacerbated respiratory disease (AERD) and the non-AERD subgroups.

Javad Nazari, Faezeh Shahba, Negin Jafariaghdam, Saleh Mohebbi, Saba Arshi, Mohammad Hassan Bemanian, Morteza Fallahpour, Sima Shokri, Fatemeh Atashrazm, Saeed Amini and 5 more

Abstract read
In one paragraph

Article in Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology, 2024. 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
–field-weighted citation impact
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.

  1. Article
  2. Review
  3. Review
  4. Multi-omics integration andFrontiers in immunology · 2026
    Article
  5. Article
  6. Review
  7. Review
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.

Javad NazariImmunology Research Center, Institute of Immunology and Infectious Diseases, Iran University of Medical Sciences, Tehran, Iran.
Faezeh ShahbaImmunology Research Center, Institute of Immunology and Infectious Diseases, Iran University of Medical Sciences, Tehran, Iran.
Negin JafariaghdamImmunology Research Center, Institute of Immunology and Infectious Diseases, Iran University of Medical Sciences, Tehran, Iran.
Saleh MohebbiSkull Base Research Center, Five Sense Health Institute, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.
Saba ArshiDepartment of Allergy and Clinical Immunology, Rasool-e-Akram Hospital, Iran University of Medical Sciences, Tehran, 14456 13131, Iran.
Mohammad Hassan BemanianDepartment of Allergy and Clinical Immunology, Rasool-e-Akram Hospital, Iran University of Medical Sciences, Tehran, 14456 13131, Iran.
Morteza FallahpourDepartment of Allergy and Clinical Immunology, Rasool-e-Akram Hospital, Iran University of Medical Sciences, Tehran, 14456 13131, Iran.
Sima ShokriDepartment of Allergy and Clinical Immunology, Rasool-e-Akram Hospital, Iran University of Medical Sciences, Tehran, 14456 13131, Iran.
Fatemeh AtashrazmDepartment of Allergy and Clinical Immunology, Rasool-e-Akram Hospital, Iran University of Medical Sciences, Tehran, 14456 13131, Iran.
Saeed AminiDepartment of Public Health, Khomein University of Medical Sciences, Khomein, Iran.
Maryam RoomianiENT and Head and Neck Research Center and Department, Firoozgar Hospital, Five Senses Health Research Institute, Iran University of Medical Sciences, Tehran, Iran.
Mahnaz JameeLaboratory for Pediatric Immunology, Department of Pediatrics, Willem-Alexander Children's Hospital, Leiden University Medical center, Leiden, Netherlands.
Pegah BabaheidarianDepartment of Pathology, Rasool-e-Akram Hospital, Iran University of Medical Sciences, Tehran, Iran.
Majid KhoshmirsafaImmunology Research Center, Institute of Immunology and Infectious Diseases, Iran University of Medical Sciences, Tehran, Iran. khoshmirsafa.m@iums.ac.ir.ORCID http://orcid.org/0000-0002-1843-8372
Mohammad NabaviDepartment of Allergy and Clinical Immunology, Rasool-e-Akram Hospital, Iran University of Medical Sciences, Tehran, 14456 13131, Iran. m.nabavi44@yahoo.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundChronic Rhinosinusitis (CRS) is a paranasal sinus inflammatory disease and is divided into two subgroups defined as CRS with nasal polyps (CRSwNP) and CRS without nasal polyps (CRSsNP). CRSwNP displays a T helper (Th)2 biased phenotype, and based on sensitivity or tolerance to aspirin or non-steroidal anti-inflammatory drugs (NSAID), is further subdivided into Aspirin-exacerbated respiratory disease (AERD) and non-AERD groups. Considering the challenge of diagnosis and treatment in patients with CRSwNP, particularly the AERD subtype, and the significance of endotyping in these patients, we examined the immune profile and endotyping based on gene expression analysis in the AERD and the non-AERD groups of patients with CRSwNP. MATERIAL AND

methodIn this study, 21 patients were enrolled and were categorized into AERD (N = 10) and non-AERD (N = 11) groups based on their sensitivity to aspirin. After the special washing period, nasal polyps were biopsied in both groups, and the infiltration of eosinophils, neutrophils, plasma cells, and lymphocytes was compared between the AERD and the non-AERD groups. Also, gene expression levels of transcription factors including Tbet, GATA3, RoRγt, and FoxP3 and inflammatory cytokines including interleukin (IL)1β, IL1RAP (IL1 receptor accessory protein), IL2, IL4, IL5, IL10, IL13, IL17, TNFα, and IFNγ were investigated by quantitative Real-time PCR (qRT-PCR). Statistical analyses were performed using analytical tests including Kolmogorov-Smirnov, Mann-Whitney, and T-test. A P value less than 0.05 was considered statistically significant.

resultsThe mean ± SD age of the studied groups was 37 ± 8.7 years old (21-50) for the AERD, and 40.4 ± 7.7 years old (31-52) for the non-AERD. LMS/EPOS/SNOT scores and pulmonary function tests showed no difference between the two groups. Serum immunoglobulin E (IgE) levels were found to be higher in patients with AERD (p = 0.04), however, the peripheral blood counts of eosinophils were comparable in the two groups. In the histopathologic analysis, the AERD group showed higher percentages of eosinophils (p = 0.04), neutrophils (p = 0.04), and plasma cells (p = 0.04) than the non-AERD group. Additionally, the gene expression levels of GATA3 (p = 0.001), IL4 (p = 0.04), IL5 (p = 0.007), and IL17 (p = 0.03) were significantly higher in the AERD than the non-AERD groups.

conclusionHigher gene expression levels of GATA3, IL4, IL5, and IL17 were observed in the AERD group compared with the non-AERD group. These findings point to distinct patterns of inflammation in patients with AERD, with a predominance of Th2 inflammation.

Identifiers

PMID38360807
PMCPMC10870654

What Socratic holds

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Registered trials

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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 Socratic graph.