Evidence map›Paper›PMID 35327420›Full record

ArticleBiomedicines2022

Immune-Mediated Inflammatory Responses of Alveolar Epithelial Cells: Implications for COVID-19 Lung Pathology.

Amelia Barilli, Rossana Visigalli, Francesca Ferrari, Massimiliano G Bianchi, Valeria Dall'Asta, Bianca Maria Rotoli

Open access · goldAbstract read
In one paragraph

Article in Biomedicines, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
4.1field-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

21 citing papers in PubMed, 27 citations in OpenAlex.

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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

6 authors at 1 institution in 1 country.

Amelia BarilliLaboratory of General Pathology, Department of Medicine and Surgery, University of Parma, 43125 Parma, Italy.ORCID 0000-0002-2256-0530
Rossana VisigalliLaboratory of General Pathology, Department of Medicine and Surgery, University of Parma, 43125 Parma, Italy.
Francesca FerrariLaboratory of General Pathology, Department of Medicine and Surgery, University of Parma, 43125 Parma, Italy.
Massimiliano G BianchiLaboratory of General Pathology, Department of Medicine and Surgery, University of Parma, 43125 Parma, Italy.
Valeria Dall'AstaLaboratory of General Pathology, Department of Medicine and Surgery, University of Parma, 43125 Parma, Italy.ORCID 0000-0001-8540-0916
Bianca Maria RotoliLaboratory of General Pathology, Department of Medicine and Surgery, University of Parma, 43125 Parma, Italy.
University of Parma · IT

Funding

Ministry of Education, Universities and Research 2017R5ZE2C
6 · The paper itself

Abstract

backgroundClinical and experimental evidence point to a dysregulated immune response caused by SARS-CoV-2 as the primary mechanism of lung disease in COVID-19. However, the pathogenic mechanisms underlying COVID-19-associated ARDS (Acute Respiratory Distress Syndrome) remain incompletely understood. This study aims to explore the inflammatory responses of alveolar epithelial cells to either the spike S1 protein or to a mixture of cytokines secreted by S1-activated macrophages. METHODS AND

resultsThe exposure of alveolar A549 cells to supernatants from spike-activated macrophages caused a further release of inflammatory mediators, with IL-8 reaching massive concentrations. The investigation of the molecular pathways indicated that NF-kB is involved in the transcription of IP-10 and RANTES, while STATs drive the expression of all the cytokines/chemokines tested, with the exception of IL-8 which is regulated by AP-1. Cytokines/chemokines produced by spike-activated macrophages are also likely responsible for the observed dysfunction of barrier integrity in Human Alveolar Epithelial Lentivirus-immortalized cells (hAELVi), as demonstrated by an increased permeability of the monolayers to mannitol, a marked decrease of TEER and a disorganization of claudin-7 distribution.

conclusionUpon exposure to supernatants from S1-activated macrophages, A549 cells act both as targets and sources of cytokines/chemokines, suggesting that alveolar epithelium along with activated macrophages may orchestrate lung inflammation and contribute to alveolar injury, a hallmark of ARDS.

Indexed as

chemokinesCOVID-19cytokinesepithelial barrier dysfunctionhuman alveolar epithelial cellshuman macrophagesIL-8

Identifiers

PMID35327420
PMCPMC8945544
OpenAlexW4221068601

What OpenQuestion holds

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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.