The pathogenic role of epithelial and endothelial cells in early-phase COVID-19 pneumonia: victims and partners in crime

Current understanding of the complex pathogenesis of COVID-19 interstitial pneumonia pathogenesis in the light of biopsies carried out in early/moderate phase and histology data obtained at postmortem analysis is discussed. In autopsies the most observed pattern is diffuse alveolar damage with alveo...

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Published inModern pathology Vol. 34; no. 8; pp. 1444 - 1455
Main Authors Chilosi, Marco, Poletti, Venerino, Ravaglia, Claudia, Rossi, Giulio, Dubini, Alessandra, Piciucchi, Sara, Pedica, Federica, Bronte, Vincenzo, Pizzolo, Giovanni, Martignoni, Guido, Doglioni, Claudio
Format Journal Article
LanguageEnglish
Published New York Elsevier Inc 01.08.2021
Nature Publishing Group US
Elsevier Limited
Subjects
13/51
631/250/254
692/420/254
Alveoli
B7-H1 Antigen - metabolism
Biopsy
Cell Communication
Coronaviruses
COVID-19
COVID-19 - metabolism
COVID-19 - mortality
COVID-19 - pathology
COVID-19 - virology
Cytokines - metabolism
Endothelial cells
Endothelial Cells - metabolism
Endothelial Cells - pathology
Endothelial Cells - virology
Epithelial Cells - metabolism
Epithelial Cells - pathology
Epithelial Cells - virology
Humans
Hyperplasia
Immune checkpoint
Indoleamine-Pyrrole 2,3,-Dioxygenase - metabolism
Laboratory Medicine
Lung - metabolism
Lung - pathology
Lung - virology
Medicine
Medicine & Public Health
Pathogenesis
Pathology
PD-L1 protein
Phosphorylation
Pneumonia
Prognosis
Respiratory failure
Review
Review Article
Severe acute respiratory syndrome coronavirus 2
Signal Transduction
Stat3 protein
STAT3 Transcription Factor - metabolism
Thromboembolism
Online AccessGet full text

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Abstract Current understanding of the complex pathogenesis of COVID-19 interstitial pneumonia pathogenesis in the light of biopsies carried out in early/moderate phase and histology data obtained at postmortem analysis is discussed. In autopsies the most observed pattern is diffuse alveolar damage with alveolar-epithelial type-II cell hyperplasia, hyaline membranes, and frequent thromboembolic disease. However, these observations cannot explain some clinical, radiological and physiopathological features observed in SARS-CoV-2 interstitial pneumonia, including the occurrence of vascular enlargement on CT and preserved lung compliance in subjects even presenting with or developing respiratory failure. Histological investigation on early-phase pneumonia on perioperative samples and lung biopsies revealed peculiar morphological and morpho-phenotypical changes including hyper-expression of phosphorylated STAT3 and immune checkpoint molecules (PD-L1 and IDO) in alveolar-epithelial and endothelial cells. These features might explain in part these discrepancies.
AbstractList Current understanding of the complex pathogenesis of COVID-19 interstitial pneumonia pathogenesis in the light of biopsies carried out in early/moderate phase and histology data obtained at postmortem analysis is discussed. In autopsies the most observed pattern is diffuse alveolar damage with alveolar-epithelial type-II cell hyperplasia, hyaline membranes, and frequent thromboembolic disease. However, these observations cannot explain some clinical, radiological and physiopathological features observed in SARS-CoV-2 interstitial pneumonia, including the occurrence of vascular enlargement on CT and preserved lung compliance in subjects even presenting with or developing respiratory failure. Histological investigation on early-phase pneumonia on perioperative samples and lung biopsies revealed peculiar morphological and morpho-phenotypical changes including hyper-expression of phosphorylated STAT3 and immune checkpoint molecules (PD-L1 and IDO) in alveolar-epithelial and endothelial cells. These features might explain in part these discrepancies.Current understanding of the complex pathogenesis of COVID-19 interstitial pneumonia pathogenesis in the light of biopsies carried out in early/moderate phase and histology data obtained at postmortem analysis is discussed. In autopsies the most observed pattern is diffuse alveolar damage with alveolar-epithelial type-II cell hyperplasia, hyaline membranes, and frequent thromboembolic disease. However, these observations cannot explain some clinical, radiological and physiopathological features observed in SARS-CoV-2 interstitial pneumonia, including the occurrence of vascular enlargement on CT and preserved lung compliance in subjects even presenting with or developing respiratory failure. Histological investigation on early-phase pneumonia on perioperative samples and lung biopsies revealed peculiar morphological and morpho-phenotypical changes including hyper-expression of phosphorylated STAT3 and immune checkpoint molecules (PD-L1 and IDO) in alveolar-epithelial and endothelial cells. These features might explain in part these discrepancies.
Current understanding of the complex pathogenesis of COVID-19 interstitial pneumonia pathogenesis in the light of biopsies carried out in early/moderate phase and histology data obtained at postmortem analysis is discussed. In autopsies the most observed pattern is diffuse alveolar damage with alveolar-epithelial type-II cell hyperplasia, hyaline membranes, and frequent thromboembolic disease. However, these observations cannot explain some clinical, radiological and physiopathological features observed in SARS-CoV-2 interstitial pneumonia, including the occurrence of vascular enlargement on CT and preserved lung compliance in subjects even presenting with or developing respiratory failure. Histological investigation on early-phase pneumonia on perioperative samples and lung biopsies revealed peculiar morphological and morpho-phenotypical changes including hyper-expression of phosphorylated STAT3 and immune checkpoint molecules (PD-L1 and IDO) in alveolar-epithelial and endothelial cells. These features might explain in part these discrepancies.
Author Chilosi, Marco
Poletti, Venerino
Pizzolo, Giovanni
Rossi, Giulio
Dubini, Alessandra
Bronte, Vincenzo
Piciucchi, Sara
Martignoni, Guido
Doglioni, Claudio
Ravaglia, Claudia
Pedica, Federica
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/33883694$$D View this record in MEDLINE/PubMed
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ContentType Journal Article
Copyright 2021 United States & Canadian Academy of Pathology
The Author(s), under exclusive licence to United States & Canadian Academy of Pathology 2021
2021. The Author(s), under exclusive licence to United States & Canadian Academy of Pathology.
The Author(s), under exclusive licence to United States & Canadian Academy of Pathology 2021.
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– notice: The Author(s), under exclusive licence to United States & Canadian Academy of Pathology 2021
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– notice: The Author(s), under exclusive licence to United States & Canadian Academy of Pathology 2021.
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Issue 8
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Snippet Current understanding of the complex pathogenesis of COVID-19 interstitial pneumonia pathogenesis in the light of biopsies carried out in early/moderate phase...
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SubjectTerms 13/51
631/250/254
692/420/254
Alveoli
B7-H1 Antigen - metabolism
Biopsy
Cell Communication
Coronaviruses
COVID-19
COVID-19 - metabolism
COVID-19 - mortality
COVID-19 - pathology
COVID-19 - virology
Cytokines - metabolism
Endothelial cells
Endothelial Cells - metabolism
Endothelial Cells - pathology
Endothelial Cells - virology
Epithelial Cells - metabolism
Epithelial Cells - pathology
Epithelial Cells - virology
Humans
Hyperplasia
Immune checkpoint
Indoleamine-Pyrrole 2,3,-Dioxygenase - metabolism
Laboratory Medicine
Lung - metabolism
Lung - pathology
Lung - virology
Medicine
Medicine & Public Health
Pathogenesis
Pathology
PD-L1 protein
Phosphorylation
Pneumonia
Prognosis
Respiratory failure
Review
Review Article
Severe acute respiratory syndrome coronavirus 2
Signal Transduction
Stat3 protein
STAT3 Transcription Factor - metabolism
Thromboembolism
Title The pathogenic role of epithelial and endothelial cells in early-phase COVID-19 pneumonia: victims and partners in crime
URI https://dx.doi.org/10.1038/s41379-021-00808-8
https://link.springer.com/article/10.1038/s41379-021-00808-8
https://www.ncbi.nlm.nih.gov/pubmed/33883694
https://www.proquest.com/docview/2553617069
https://www.proquest.com/docview/2516842945
https://pubmed.ncbi.nlm.nih.gov/PMC8058579
Volume 34
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