Evidence map›Paper›PMID 34404754›Full record

ReviewThorax2022

Respiratory epithelial cell responses to SARS-CoV-2 in COVID-19.

James P Bridges, Eszter K Vladar, Hua Huang, Robert J Mason

Open access · greenAbstract readReview
In one paragraph

Review in Thorax, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 105 papers.

0numbers the graph read from it
0cells of the map it votes in
105citing papers in PubMed
19.8field-weighted citation impact, top 1% 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

105 citing papers in PubMed, 159 citations in OpenAlex.

  1. Trial
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  9. Detection ofFrontiers in cellular and infection microbiology · 2026
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45 more citing papers are in PubMed but not listed here.

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

4 authors at 2 institutions in 1 country.

James P BridgesDepartment of Medicine, Division of Pulmonary, Critical Care and Sleep Medicine, National Jewish Health, Denver, Colorado, USA bridgesj@njhealth.org.ORCID 0000-0002-4815-117X
Eszter K VladarDepartment of Medicine, Division of Pulmonary Sciences and Critical Care Medicine and Department of Cell and Developmental Biology, University of Colorado School of Medicine, Aurora, Colorado, USA.ORCID 0000-0002-4160-8894
Hua HuangDepartment of Immunology and Genomic Medicine, National Jewish Health, Denver, Colorado, USA.
Robert J MasonDepartment of Medicine, Division of Pulmonary, Critical Care and Sleep Medicine, National Jewish Health, Denver, Colorado, USA.
National Jewish Health · USUniversity of Colorado Denver · US

Funding

Role of GPR116 in Alveolar HomeostasisR01HL131634 · NHLBI · NATIONAL JEWISH HEALTH · PI BRIDGES, JAMES PATRICK · 2016 to 2020
$2.0M
NHLBI NIH HHS R01 HL131634
6 · The paper itself

Abstract

COVID-19 has different clinical stages, and effective therapy depends on the location and extent of the infection. The purpose of this review is to provide a background for understanding the progression of the disease throughout the pulmonary epithelium and discuss therapeutic options. The prime sites for infection that will be contrasted in this review are the conducting airways and the gas exchange portions of the lung. These two sites are characterised by distinct cellular composition and innate immune responses, which suggests the use of distinct therapeutic agents. In the nose, ciliated cells are the primary target cells for SARS-CoV-2 viral infection, replication and release. Infected cells shed their cilia, which disables mucociliary clearance. Evidence further points to a suppressed or incompletely activated innate immune response to SARS-CoV-2 infection in the upper airways. Asymptomatic individuals can still have a productive viral infection and infect others. In the gas exchange portion of the lung, the alveolar type II epithelial cell is the main target cell type. Cell death and marked innate immune response during infection likely contribute to alveolar damage and resultant acute respiratory distress syndrome. Alveolar infection can precipitate a hyperinflammatory state, which is the target of many therapies in severe COVID-19. Disease resolution in the lung is variable and may include scaring and long-term sequalae because the alveolar type II cells are also progenitor cells for the alveolar epithelium.

Indexed as

COVID-19Epithelial CellsHumansLungRespiratory MucosaSARS-CoV-2airway epitheliumARDSCOVID-19

Identifiers

PMID34404754
PMCPMC9273148
OpenAlexW3194430494

What OpenQuestion holds

Textmetadata
LicenceTDM
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.