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


Journal

Cytokine
ISSN: 1096-0023
Titre abrégé: Cytokine
Pays: England
ID NLM: 9005353

Informations de publication

Date de publication:
09 2023
Historique:
received: 27 09 2022
revised: 18 03 2023
accepted: 27 05 2023
medline: 11 8 2023
pubmed: 12 6 2023
entrez: 12 6 2023
Statut: ppublish

Résumé

One 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. Peripheral 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. The 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. Based 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.

Sections du résumé

BACKGROUND
One 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 METHODS
Peripheral 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.
RESULTS
The 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.
CONCLUSION
Based 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.

Identifiants

pubmed: 37307689
pii: S1043-4666(23)00126-6
doi: 10.1016/j.cyto.2023.156248
pmc: PMC10247889
pii:
doi:

Substances chimiques

Forkhead Transcription Factors 0
Interleukin-10 130068-27-8
Interleukin-17 0
MicroRNAs 0
MIRN155 microRNA, human 0
Nuclear Receptor Subfamily 1, Group F, Member 3 0
RNA, Viral 0
SOCS1 protein, human 0
Suppressor of Cytokine Signaling 1 Protein 0
Suppressor of Cytokine Signaling Proteins 0
Transforming Growth Factor beta 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

156248

Informations de copyright

Copyright © 2023 Elsevier Ltd. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Auteurs

Mohammad Sadegh Soltani-Zangbar (MS)

Student 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 Hajivalili (M)

Behbahan Faculty of Medical Sciences, Behbahan, Iran.

Danyal Daneshdoust (D)

Faculty of Medicine, Babol University of Medical Sciences, Babol, Iran.

Sara Ghadir (S)

Student Research Committee, Faculty of Medical Sciences, Babol University of Medical Sciences, Babol, Iran.

Golaleh Savari (G)

Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.

Mohammadali Zolfaghari (M)

Molecular Medicine Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.

Leili Aghebati-Maleki (L)

Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.

Solmaz Oloufi (S)

School of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran; School of Medicine, Urmia University of Medical Sciences, Urmia, Iran.

Narjes Nouri (N)

Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran; Department of Immunology, School of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran.

Naser Amini (N)

Cellular 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 Mehdizadeh (A)

Hematology and Oncology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.

Hossein Ghasemi Moghadam (H)

Hematology and Oncology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.

Ata Mahmoodpoor (A)

Department of Anesthesiology, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran.

Javad Ahmadian Heris (J)

Department of Allergy and Clinical Immunology, Pediatric Hospital, Tabriz University of Medical Sciences, Tabriz, Iran.

Mehdi Yousefi (M)

Immunology 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.

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Classifications MeSH