Introduction: SARS-CoV-2 affects part of the innate immune response and activates an inflammatory cascade stimulating the release of cytokines and chemokines, particularly within the lung. Indeed, the inflammatory response during COVID-19 is likely the cause for the development of acute respiratory distress syndrome (ARDS). Patients with mild symptoms also show significant changes on pulmonary CT-scan suggestive of severe inflammatory involvement.
Hypothesis: The overall hypothesis is that HBO is safe and reduces the inflammatory response in COVID-19 pneumonitis by attenuation of the innate immune system, increase hypoxia tolerance and thereby prevent organ failure and reduce mortality.
Evaluation Of The Hypothesis: HBO is used in clinical practice to treat inflammatory conditions but has not been scientifically evaluated for COVID-19. Experimental and empirical data suggests that HBO may reduce inflammatory response in COVID-19. However, there are concerns regarding pulmonary safety in patients with pre-existing viral pneumonitis.
Empirical Data: Anecdotes from "compassionate use" and two published case reports show promising results.
Consequences Of The Hypothesis And Discussion: Small prospective clinical trials are on the way and we are conducting a randomized clinical trial.
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http://dx.doi.org/10.1016/j.mehy.2020.110224 | DOI Listing |
Cardiovasc Toxicol
January 2025
Department of Cadre Ward, The First Affiliated Hospital of Harbin Medical University, No. 23, Postal Street, Harbin, 150001, Heilongjiang, PR China.
Atherosclerosis risk is elevated in diabetic patients, but the underlying mechanism such as the involvement of macrophages remains unclear. Here, we investigated the underlying mechanism related to the pro-inflammatory activation of macrophages in the development of diabetic atherosclerosis. Bioinformatics tools were used to analyze the macrophage-related transcriptome differences in patients with atherosclerosis and diabetic mice.
View Article and Find Full Text PDFJ Infect Dev Ctries
December 2024
Students' Research Committee, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran.
Introduction: Inflammation plays a role in coronavirus disease 2019 (COVID-19) pathophysiology and anti-inflammatory drugs may help reduce the disease severity. Levamisole is an anthelmintic drug with immunomodulatory and possible antiviral effects. This study aimed to evaluate the role of levamisole in the treatment of patients with COVID-19.
View Article and Find Full Text PDFJ Infect Dev Ctries
December 2024
Intensive Care Unit, Columbia Asia Hospital, Semarang, Indonesia.
Introduction: Hemoperfusion (HP), a blood filtration method targeting the removal of toxins and inflammatory elements, was investigated in this study. The objective was to present the observations in four individuals with confirmed COVID-19 who underwent several rounds of HP utilizing the HA330 cartridge at a hospital in Indonesia.
Case Studies: We report four cases of COVID-19 patients who underwent HP.
Semin Immunopathol
January 2025
Institute for Clinical Chemistry and Laboratory Medicine, Faculty of Medicine and University Hospital Carl Gustav Carus, Technische Universität Dresden, Fetscherstrasse 74, 01307, Dresden, Germany.
Metabolic flexibility is key for the function of myeloid cells. Arginine metabolism is integral to the regulation of myeloid cell responses. Nitric oxide (NO) production from arginine is vital for the antimicrobial and pro-inflammatory responses.
View Article and Find Full Text PDFSci Rep
January 2025
Department of Biomedical Engineering, University of Rochester, Rochester, NY, USA.
The aberrant vascular response associated with tendon injury results in circulating immune cell infiltration and a chronic inflammatory feedback loop leading to poor healing outcomes. Studying this dysregulated tendon repair response in human pathophysiology has been historically challenging due to the reliance on animal models. To address this, our group developed the human tendon-on-a-chip (hToC) to model cellular interactions in the injured tendon microenvironment; however, this model lacked the key element of physiological flow in the vascular compartment.
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