Evidence map›Paper›PMID 35630492›Full record

ReviewMicroorganisms2022

SARS CoV-2-Induced Viral Sepsis: The Role of Gut Barrier Dysfunction.

Stelios F Assimakopoulos, Gerasimos Eleftheriotis, Maria Lagadinou, Vassilios Karamouzos, Periklis Dousdampanis, Georgios Siakallis, Markos Marangos

Open access · goldAbstract readReview
In one paragraph

Review in Microorganisms, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
4.0field-weighted citation impact, top 5% 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

25 citing papers in PubMed, 44 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Review
  11. Observational
  12. Review
  13. Review
  14. Progress in the study of the correlation between sepsis and intestinal microecology.Frontiers in cellular and infection microbiology · 2024
    Review
  15. Article
  16. Review
  17. Review
  18. Review
  19. Review
  20. 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

7 authors at 3 institutions in 2 countries.

Stelios F AssimakopoulosDivision of Infectious Diseases, Department of Internal Medicine, University of Patras Medical School, 26504 Patras, Greece.ORCID 0000-0002-6901-3681
Gerasimos EleftheriotisDivision of Infectious Diseases, Department of Internal Medicine, University of Patras Medical School, 26504 Patras, Greece.ORCID 0000-0003-3665-2855
Maria LagadinouDivision of Infectious Diseases, Department of Internal Medicine, University of Patras Medical School, 26504 Patras, Greece.
Vassilios KaramouzosDivision of Infectious Diseases, Department of Internal Medicine, University of Patras Medical School, 26504 Patras, Greece.
Periklis DousdampanisHemodialysis Unit Kyanos Stavros, 26225 Patras, Greece.
Georgios SiakallisDepartment of Basic and Clinical Sciences, University of Nicosia Medical School, Nicosia 2408, Cyprus.
Markos MarangosDivision of Infectious Diseases, Department of Internal Medicine, University of Patras Medical School, 26504 Patras, Greece.
University of Patras · GRKyanous Stavros Hospital · GRUniversity of Nicosia · CY

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A considerable proportion of patients with severe COVID-19 meet Sepsis-3 criteria and share common pathophysiological mechanisms of multiorgan injury with bacterial sepsis, in absence of secondary bacterial infections, a process characterized as "viral sepsis". The intestinal barrier exerts a central role in the pathophysiological sequence of events that lead from SARS-CoV-2 infection to severe systemic complications. Accumulating evidence suggests that SARS-CoV-2 disrupts the integrity of the biological, mechanical and immunological gut barrier. Specifically, microbiota diversity and beneficial bacteria population are reduced, concurrently with overgrowth of pathogenic bacteria (dysbiosis). Enterocytes' tight junctions (TJs) are disrupted, and the apoptotic death of intestinal epithelial cells is increased leading to increased gut permeability. In addition, mucosal CD4(+) and CD8(+) T cells, Th17 cells, neutrophils, dendritic cells and macrophages are activated, and T-regulatory cells are decreased, thus promoting an overactivated immune response, which further injures the intestinal epithelium. This dysfunctional gut barrier in SARS-CoV-2 infection permits the escape of luminal bacteria, fungi and endotoxin to normally sterile extraintestinal sites and the systemic circulation. Pre-existing gut barrier dysfunction and endotoxemia in patients with comorbidities including cardiovascular disease, obesity, diabetes and immunosuppression predisposes to aggravated endotoxemia. Bacterial and endotoxin translocation promote the systemic inflammation and immune activation, which characterize the SARS-CoV-2 induced "viral sepsis" syndrome associated with multisystemic complications of severe COVID-19.

Indexed as

bacterial translocationCOVID-19endotoxinintestinal barriermicrobial translocationmicrobiotaSARS-CoV-2sepsistight junctionsviral sepsis

Identifiers

PMID35630492
PMCPMC9143860
OpenAlexW4280575933

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.