ArticleRespiratory research2022
Pulmonary vascular inflammation with fatal coronavirus disease 2019 (COVID-19): possible role for the NLRP3 inflammasome.
Article in Respiratory research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 30 citations in OpenAlex.
- Triple-Action Antioxidant, Antiviral, and Immunomodulatory Effects of Hypericum perforatum Against SARS-CoV-2 Using Chemical-Based and In Vitro Methods.Plant foods for human nutrition (Dordrecht, Netherlands) · 2026Article
- Cardiovascular sequelae of Long COVID: immune dysregulation inflammation as central drivers.Frontiers in immunology · 2026Review
- Circadian Control of Pulmonary Endothelial Signaling Occurs via the NADPH Oxidase 2-NLRP3 Pathway.Journal of biological rhythms · 2025Article
- A feedback loop between DNA damage, genomic instability, and cytoplasmic DNA sensing contributes to cytokine production in COVID-19.Archives of virology · 2025Review
- Excess respiratory, circulatory, neoplasm, and other mortality rates during the Covid-19 pandemic in the EU and their implications.Epidemiology and infection · 2025Article
- Human pulmonary microvascular endothelial cells respond to DAMPs from injured renal tubular cells.Pulmonary circulation · 2024Article
- Viral uptake and pathophysiology of the lung endothelial cells in age-associated severe SARS-CoV-2 infection models.Aging cell · 2024Article
- Reactive oxygen species in endothelial signaling in COVID-19: Protective role of the novel peptide PIP-2.PloS one · 2024Article
- Epidemiology, Symptoms and Pathophysiology of Long Covid Complications.Journal of cellular immunology · 2024Article
- Vitamin D regulates COVID-19 associated severity by suppressing the NLRP3 inflammasome pathway.PloS one · 2024Article
- Caspase-1 activation, IL-1/IL-6 signature and IFNγ-induced chemokines in lungs of COVID-19 patients.Frontiers in immunology · 2024Article
- NLRP3 inflammasome and interleukin-1 contributions to COVID-19-associated coagulopathy and immunothrombosis.Cardiovascular research · 2023Article
- The effects and mechanisms of the anti-COVID-19 traditional Chinese medicine, Dehydroandrographolide from Andrographis paniculata (Burm.f.) Wall, on acute lung injury by the inhibition of NLRP3-mediated pyroptosis.Phytomedicine : international journal of phytotherapy and phytopharmacology · 2023Article
- Cellular Sensors and Viral Countermeasures: A Molecular Arms Race between Host and SARS-CoV-2.Viruses · 2023Review
- Inflammasomes: a rising star on the horizon of COVID-19 pathophysiology.Frontiers in immunology · 2023Review
- Ribavirin aerosol in hospitalized adults with respiratory distress and COVID-19: An open-label trial.Clinical and translational science · 2023Article
- Serum gasdermin D levels are associated with the chest computed tomography findings and severity of COVID-19.Respiratory investigation · 2022Article
- Symptomatology and microbiology of the gastrointestinal tract in post-COVID conditions.JGH open : an open access journal of gastroenterology and hepatology · 2022Review
- The Contribution of Gut Microbiota and Endothelial Dysfunction in the Development of Arterial Hypertension in Animal Models and in Humans.International journal of molecular sciences · 2022Review
- Inflammasome activation at the crux of severe COVID-19.Nature reviews. Immunology · 2021Review
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9 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundPulmonary hyperinflammation is a key event with SARS-CoV-2 infection. Acute respiratory distress syndrome (ARDS) that often accompanies COVID-19 appears to have worse outcomes than ARDS from other causes. To date, numerous lung histological studies in cases of COVID-19 have shown extensive inflammation and injury, but the extent to which these are a COVID-19 specific, or are an ARDS and/or mechanical ventilation (MV) related phenomenon is not clear. Furthermore, while lung hyperinflammation with ARDS (COVID-19 or from other causes) has been well studied, there is scarce documentation of vascular inflammation in COVID-19 lungs.
methodsLung sections from 8 COVID-19 affected and 11 non-COVID-19 subjects, of which 8 were acute respiratory disease syndrome (ARDS) affected (non-COVID-19 ARDS) and 3 were from subjects with non-respiratory diseases (non-COVID-19 non-ARDS) were H&E stained to ascertain histopathological features. Inflammation along the vessel wall was also monitored by expression of NLRP3 and caspase 1.
resultsIn lungs from COVID-19 affected subjects, vascular changes in the form of microthrombi in small vessels, arterial thrombosis, and organization were extensive as compared to lungs from non-COVID-19 (i.e., non-COVID-19 ARDS and non-COVID-19 non-ARDS) affected subjects. The expression of NLRP3 pathway components was higher in lungs from COVID-19 ARDS subjects as compared to non-COVID-19 non-ARDS cases. No differences were observed between COVID-19 ARDS and non-COVID-19 ARDS lungs.
conclusionVascular changes as well as NLRP3 inflammasome pathway activation were not different between COVID-19 and non-COVID-19 ARDS suggesting that these responses are not a COVID-19 specific phenomenon and are possibly more related to respiratory distress and associated strategies (such as MV) for treatment.
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