Evidence map›Paper›PMID 35128349›Full record

ArticleiScience2022

The interplay between SARS-CoV-2 infected airway epithelium and immune cells modulates regulatory/inflammatory signals.

Veronica Bordoni, Giulia Matusali, Davide Mariotti, Manuela Antonioli, Eleonora Cimini, Alessandra Sacchi, Eleonora Tartaglia, Rita Casetti, Germana Grassi, Stefania Notari and 5 more

Open access · goldAbstract read
In one paragraph

Article in iScience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.5field-weighted citation impact, top 38% 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

4 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Methods and Models for StudyingInternational journal of molecular sciences · 2024
    Review
  3. Article
  4. 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

15 authors at 1 institution in 1 country.

Veronica BordoniNational Institute for Infectious Diseases Lazzaro Spallanzani-IRCCS, Via Portuense, 292, Rome 00149, Italy.
Giulia MatusaliNational Institute for Infectious Diseases Lazzaro Spallanzani-IRCCS, Via Portuense, 292, Rome 00149, Italy.
Davide MariottiNational Institute for Infectious Diseases Lazzaro Spallanzani-IRCCS, Via Portuense, 292, Rome 00149, Italy.
Manuela AntonioliNational Institute for Infectious Diseases Lazzaro Spallanzani-IRCCS, Via Portuense, 292, Rome 00149, Italy.
Eleonora CiminiNational Institute for Infectious Diseases Lazzaro Spallanzani-IRCCS, Via Portuense, 292, Rome 00149, Italy.
Alessandra SacchiNational Institute for Infectious Diseases Lazzaro Spallanzani-IRCCS, Via Portuense, 292, Rome 00149, Italy.
Eleonora TartagliaNational Institute for Infectious Diseases Lazzaro Spallanzani-IRCCS, Via Portuense, 292, Rome 00149, Italy.
Rita CasettiNational Institute for Infectious Diseases Lazzaro Spallanzani-IRCCS, Via Portuense, 292, Rome 00149, Italy.
Germana GrassiNational Institute for Infectious Diseases Lazzaro Spallanzani-IRCCS, Via Portuense, 292, Rome 00149, Italy.
Stefania NotariNational Institute for Infectious Diseases Lazzaro Spallanzani-IRCCS, Via Portuense, 292, Rome 00149, Italy.
Concetta CastillettiNational Institute for Infectious Diseases Lazzaro Spallanzani-IRCCS, Via Portuense, 292, Rome 00149, Italy.
Gian Maria FimiaNational Institute for Infectious Diseases Lazzaro Spallanzani-IRCCS, Via Portuense, 292, Rome 00149, Italy.
Maria Rosaria CapobianchiNational Institute for Infectious Diseases Lazzaro Spallanzani-IRCCS, Via Portuense, 292, Rome 00149, Italy.
Giuseppe IppolitoNational Institute for Infectious Diseases Lazzaro Spallanzani-IRCCS, Via Portuense, 292, Rome 00149, Italy.
Chiara AgratiNational Institute for Infectious Diseases Lazzaro Spallanzani-IRCCS, Via Portuense, 292, Rome 00149, Italy.
Istituto Nazionale per le Malattie Infettive Lazzaro Spallanzani · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

To assess the cross-talk between immune cells and respiratory tract during SARS-CoV-2 infection, we analyzed the relationships between the inflammatory response induced by SARS-CoV-2 replication and immune cells phenotype in a reconstituted organotypic human airway epithelium (HAE). The results indicated that immune cells failed to inhibit SARS-CoV-2 replication in the HAE model. In contrast, immune cells strongly affected the inflammatory profile induced by SARS-CoV-2 infection, dampening the production of several immunoregulatory/inflammatory signals (e.g., IL-35, IL-27, and IL-34). Moreover, these mediators were found inversely correlated with innate immune cell frequency (NK and γδ T cells) and directly with CD8 T cells. The enriched signals associated with NK and CD8 T cells highlighted the modulation of pathways induced by SARS-CoV-2 infected HAE. These findings are useful to depict the cell-cell communication mechanisms necessary to develop novel therapeutic strategies aimed to promote an effective immune response.

Indexed as

ImmunologyVirology

Identifiers

PMID35128349
PMCPMC8802491
OpenAlexW4210697942

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.