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Cell ; 184(26): 6243-6261.e27, 2021 12 22.
Article in English | MEDLINE | ID: covidwho-1536467


COVID-19-induced "acute respiratory distress syndrome" (ARDS) is associated with prolonged respiratory failure and high mortality, but the mechanistic basis of lung injury remains incompletely understood. Here, we analyze pulmonary immune responses and lung pathology in two cohorts of patients with COVID-19 ARDS using functional single-cell genomics, immunohistology, and electron microscopy. We describe an accumulation of CD163-expressing monocyte-derived macrophages that acquired a profibrotic transcriptional phenotype during COVID-19 ARDS. Gene set enrichment and computational data integration revealed a significant similarity between COVID-19-associated macrophages and profibrotic macrophage populations identified in idiopathic pulmonary fibrosis. COVID-19 ARDS was associated with clinical, radiographic, histopathological, and ultrastructural hallmarks of pulmonary fibrosis. Exposure of human monocytes to SARS-CoV-2, but not influenza A virus or viral RNA analogs, was sufficient to induce a similar profibrotic phenotype in vitro. In conclusion, we demonstrate that SARS-CoV-2 triggers profibrotic macrophage responses and pronounced fibroproliferative ARDS.

COVID-19/pathology , COVID-19/virology , Idiopathic Pulmonary Fibrosis/pathology , Idiopathic Pulmonary Fibrosis/virology , Macrophages/pathology , Macrophages/virology , SARS-CoV-2/physiology , Antigens, CD/metabolism , Antigens, Differentiation, Myelomonocytic/metabolism , COVID-19/diagnostic imaging , Cell Communication , Cohort Studies , Fibroblasts/pathology , Gene Expression Regulation , Humans , Idiopathic Pulmonary Fibrosis/diagnostic imaging , Idiopathic Pulmonary Fibrosis/genetics , Mesenchymal Stem Cells/pathology , Phenotype , Proteome/metabolism , Receptors, Cell Surface/metabolism , Respiratory Distress Syndrome/diagnostic imaging , Respiratory Distress Syndrome/pathology , Respiratory Distress Syndrome/virology , Tomography, X-Ray Computed , Transcription, Genetic
Tuberk Toraks ; 68(4): 419-429, 2020 Dec.
Article in Turkish | MEDLINE | ID: covidwho-1067902


Though it has been 8 months since the beginning of COVID-19 pandemic, number of cases and deaths are still seriously increasing. We still don't have enough evidence about the prognosis of patients who had COVID-19 pneumonia. In long term follow up we wonder if they will have rapid FVC decline, widespread fibrosis in computed tomography, loss in quality of life or increased mortality that we experience in idiopathic pulmonary fibrosis, chronic hypersensitivity pneumonia or autoimmune interstitial lung diseases. However, in elderly patients less severe dysfunction or non-progressive-fibrosis can cause morbidity and mortality. Therefore, if we consider millions of people who are affected by COVID-19, even a rare complication can cause serious health problem in social scale. Because of the importance of this issue randomized controlled trials should be rapidly planned on post-COVID fibrosis, COVID associated thrombosis, risk factors, prevention and treatment (1). In this review, the frequency, clinical importance, prevention and treatment of possible long-term sequels of COVID-19 pneumonia (pulmonary fibrosis, pulmonary embolism and pulmonary hypertension) will be discussed.

COVID-19/epidemiology , Idiopathic Pulmonary Fibrosis/prevention & control , Pandemics , SARS-CoV-2 , COVID-19/complications , Humans , Idiopathic Pulmonary Fibrosis/complications , Idiopathic Pulmonary Fibrosis/diagnostic imaging , Prognosis , Risk Factors , Tomography, X-Ray Computed