Evidence map›Paper›PMID 36174833›Full record

ArticleMicrobial pathogenesis2022

Downregulation of ACE, AGTR1, and ACE2 genes mediating SARS-CoV-2 pathogenesis by gut microbiota members and their postbiotics on Caco-2 cells.

Sara Ahmadi Badi, Amin Malek, Alessandro Paolini, Mahya Rouhollahi Masoumi, Seyed Amirhesam Seyedi, Amir Amanzadeh, Andrea Masotti, Shohreh Khatami, Seyed Davar Siadat

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Article in Microbial pathogenesis, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

13 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
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  6. The pediatric gut bacteriome and virome in response to SARS-CoV-2 infection.Frontiers in cellular and infection microbiology · 2024
    Article
  7. The effect ofJournal of diabetes and metabolic disorders · 2023
    Article
  8. Dynamics of the Microbiota and Its Relationship with Post-COVID-19 Syndrome.International journal of molecular sciences · 2023
    Review
  9. Article
  10. Review
  11. Review
  12. COVID-19 and Gut Injury.Nutrients · 2022
    Review
  13. 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

9 authors at 3 institutions in 2 countries.

Sara Ahmadi BadiMicrobiology Research Center, Pasteur Institute of Iran, Tehran, Iran; Mycobacteriology and Pulmonary Research Department, Pasteur Institute of Iran, Tehran, Iran. Electronic address: sarahmadi@gmail.com.
Amin MalekMicrobiology Research Center, Pasteur Institute of Iran, Tehran, Iran; Mycobacteriology and Pulmonary Research Department, Pasteur Institute of Iran, Tehran, Iran. Electronic address: amin.malek73@yahoo.com.
Alessandro PaoliniResearch Laboratories, Bambino Gesù Children's Hospital-IRCCS, Rome, Italy. Electronic address: alepaolini86@gmail.com.
Mahya Rouhollahi MasoumiDepartment of Stem Cells and Developmental Biology, Cell Science Research Center, Royan Institute for Stem Cell Biology and Technology, ACECR, Tehran, Iran. Electronic address: mahya.r.m.1371@gmail.com.
Seyed Amirhesam SeyediMicrobiology Research Center, Pasteur Institute of Iran, Tehran, Iran; Mycobacteriology and Pulmonary Research Department, Pasteur Institute of Iran, Tehran, Iran. Electronic address: amirhesam.seyyedi@gmail.com.
Amir AmanzadehNational Cell Bank of Iran, Pasteur Institute of Iran, Tehran, Iran. Electronic address: amir_amanzadeh@yahoo.com.
Andrea MasottiResearch Laboratories, Bambino Gesù Children's Hospital-IRCCS, Rome, Italy. Electronic address: andrea.masotti@opbg.net.
Shohreh KhatamiDepartment of Biochemistry, Pasteur Institute of Iran, Tehran, Iran. Electronic address: sh-khatami@pasteur.ac.ir.
Seyed Davar SiadatMicrobiology Research Center, Pasteur Institute of Iran, Tehran, Iran; Mycobacteriology and Pulmonary Research Department, Pasteur Institute of Iran, Tehran, Iran. Electronic address: d.siadat@gmail.com.
Pasteur Institute of Iran · IRBambino Gesù Children's Hospital · ITRoyan Institute · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionCoronavirus disease-2019 (COVID-19) is a complex infection caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that can cause also gastrointestinal symptoms. There are various factors that determine the host susceptibility and severity of infection, including the renin-angiotensin system, the immune response, and the gut microbiota. In this regard, we aimed to investigate the gene expression of ACE, AGTR1, ACE2, and TMPRSS2, which mediate SARS-CoV-2 pathogenesis by Akkermansia muciniphila, Faecalibacterium prausnitzii, Bacteroides thetaiotaomicron, and Bacteroides fragilis on Caco-2 cells. Also, the enrichment analysis considering the studied genes was analyzed on raw data from the microarray analysis of COVID-19 patients. MATERIALS AND

methodsCaco-2 cells were treated with live, heat-inactivated form and cell free supernatants of A. muciniphila, F. prausnitzii, B. thetaiotaomicron and B. fragilis for overnight. After RNA extraction and cDNA synthesis, the expression of studied genes was assessed by RT-qPCR. DNA methylation of studied genes was analyzed by Partek® Genomics Suite® software on the GSE174818 dataset. We used GSE164805 and GSE166552 datasets from COVID-19 patients to perform enrichment analysis by considering the mentioned genes via GEO2R, DAVID. Finally, the related microRNAs to GO terms concerned on the studied genes were identified by miRPath.

resultsThe downregulation of ACE, AGTR1, and ACE2 genes by A. muciniphila, F. prausnitzii, B. thetaiotaomicron, and B. fragilis in live, heat-inactivated, and cell-free supernatants was reported for the first time. These genes had hypomethylated DNA status in COVID-19 patients' raw data. The highest fold enrichment in upregulated RAS pathways and immune responses belonged to ACE, AGTR1, and ACE2 by considering the protein-protein interaction network. The common miRNAs targeting the studied genes were reported as miR-124-3p and miR-26b-5p.

conclusionIn combination with our experimental data and bioinformatic analysis, we showed the potential of A. muciniphila, F. prausnitzii, B. thetaiotaomicron, and B. fragilis and their postbiotics to reduce ACE, ATR1, and ACE2 expression, which are essential genes that drive upregulated biological processes in COVID-19 patients. Accordingly, due to the potential of studied bacteria on the alteration of ACE, AGTR1, ACE2 genes expression, understanding their correlation with demonstrated miRNAs expression could be valuable. These findings suggest the importance of considering targeted gut microbiota intervention when designing the possible therapeutic strategy for controlling the COVID-19.

Indexed as

Angiotensin-Converting Enzyme 2COVID-19Gastrointestinal MicrobiomeMicroRNAsPeptidyl-Dipeptidase AReceptor, Angiotensin, Type 1Caco-2 CellsDown-RegulationHumansSARS-CoV-2ACE2 protein, humanACE protein, humanAGTR1 protein, humanAngiotensin-Converting Enzyme 2MicroRNAsPeptidyl-Dipeptidase AReceptor, Angiotensin, Type 1COVID-19Gut microbiotaPostbioticsRenin angiotensin systemSARS-CoV2

Identifiers

PMID36174833
PMCPMC9511898
OpenAlexW4297282111

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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 OpenQuestion graph.