Evidence map›Paper›PMID 37307689›Full record

ArticleCytokine2023

SARS-CoV2 infection induce miR-155 expression and skewed Th17/Treg balance by changing SOCS1 level: A clinical study.

Mohammad Sadegh Soltani-Zangbar, Mahsa Hajivalili, Danyal Daneshdoust, Sara Ghadir, Golaleh Savari, Mohammadali Zolfaghari, Leili Aghebati-Maleki, Solmaz Oloufi, Narjes Nouri, Naser Amini and 5 more

Open access · greenAbstract read
In one paragraph

Article in Cytokine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
3.5field-weighted citation impact, top 6% 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

14 citing papers in PubMed, 18 citations in OpenAlex.

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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 1 country.

Mohammad Sadegh Soltani-ZangbarStudent Research Committee, Tabriz University of Medical Sciences, Tabriz, Iran; Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran; Department of Immunology, School of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran.
Mahsa HajivaliliBehbahan Faculty of Medical Sciences, Behbahan, Iran.
Danyal DaneshdoustFaculty of Medicine, Babol University of Medical Sciences, Babol, Iran.
Sara GhadirStudent Research Committee, Faculty of Medical Sciences, Babol University of Medical Sciences, Babol, Iran.
Golaleh SavariImmunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Mohammadali ZolfaghariMolecular Medicine Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Leili Aghebati-MalekiImmunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Solmaz OloufiSchool of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran; School of Medicine, Urmia University of Medical Sciences, Urmia, Iran.
Narjes NouriImmunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran; Department of Immunology, School of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran.
Naser AminiCellular and Molecular Research Center, Iran University of Medical Sciences, Tehran, Iran; Institute of Regenerative Medicine, School of Advanced Technologies in Medicine, Iran University of Medical Sciences, Tehran, Iran.
Amir MehdizadehHematology and Oncology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Hossein Ghasemi MoghadamHematology and Oncology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Ata MahmoodpoorDepartment of Anesthesiology, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran.
Javad Ahmadian HerisDepartment of Allergy and Clinical Immunology, Pediatric Hospital, Tabriz University of Medical Sciences, Tabriz, Iran.
Mehdi YousefiImmunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran; Department of Immunology, School of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran. Electronic address: Yousefime@tbzmed.ac.ir.
Tabriz University of Medical Sciences · IRBabol University of Medical Sciences · IRIran University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundOne of the regulators in severe acute respiratory syndrome coronavirus2 (SARS-CoV2) infection is miRNAs. In COVID-19 patients, immunological responses to SARS-CoV2 infection may be impacted by miR-155, a miRNA associated to inflammation. MATERIALS AND

methodsPeripheral blood mononuclear cells (PBMCs) of 50 confirmed COVID-19 patients /Healthy Controls (HCs) was isolated by Ficoll. The frequency of T helper 17 and regulatory T cells was analyzed by flowcytometry. The RNA was extracted from each sample and after synthesis of c-DNA, the relative expression of miR-155, suppressor of cytokine signaling (SOCS-1), Signal transducer and activator of transcription 3(STAT3), and Fork Head Box Protein 3 (FoxP3) was evaluated by real-time PCR. The protein level of STAT3, FoxP3 and RORγT in the isolated PBMCs measured by western blotting. The serum level of IL-10, TGF-β, IL-17 and IL21 was assessed by ELISA method.

resultsThe population of Th17 cells showed a significant rise, whereas Treg cells reduced in COVID-19 cases. The master transcription factor of Treg (FoxP3) and Th17 (RORγT) relative expression showed the same pattern as flowcytometry. STAT3 level of expression at RNA and protein level increased in COVID-19 cases. FOXP3 and SOCS-1 proteins were down-regulated. The relative expression of miR-155, up-regulated in PBMC of COVID-19 patients and revealed a negative correlation with SOCS-1. The serum cytokine profile showed a reduction in TGF-β, on the other hand an increase was seen in IL-17, IL-21 and IL-10 in COVID-19 cases toward control group.

conclusionBased on the studies conducted in this field, it can be suggested that Th17/Treg in covid-19 patients can be affected by miR-155 and it can be considered a valuable diagnostic and prognostic factor in this disease.

Indexed as

COVID-19MicroRNAsSuppressor of Cytokine Signaling 1 ProteinTh17 CellsT-Lymphocytes, RegulatoryForkhead Transcription FactorsHumansInterleukin-10Interleukin-17Leukocytes, MononuclearNuclear Receptor Subfamily 1, Group F, Member 3RNA, ViralSARS-CoV-2Suppressor of Cytokine Signaling ProteinsTransforming Growth Factor betaForkhead Transcription FactorsInterleukin-10Interleukin-17MicroRNAsMIRN155 microRNA, humanNuclear Receptor Subfamily 1, Group F, Member 3RNA, ViralSOCS1 protein, humanSuppressor of Cytokine Signaling 1 ProteinSuppressor of Cytokine Signaling ProteinsTransforming Growth Factor betaCellular immunityMicro RNAT cellViral infection

Identifiers

PMID37307689
PMCPMC10247889
OpenAlexW4379911287

What Socratic holds

Textmetadata
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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 Socratic graph.