The Alarmin IL-33 Exacerbates Pulmonary Inflammation and Immune Dysfunction in SARS-CoV-2 Infection
SSRN, ISSN: 1556-5068
2024
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Article Description
Dysregulated host immune responses crucially contribute to the severity and poor recovery of COVID-19; yet the underlying mechanisms are not fully understood. In this study, we observed that IL-33, a damage-associated molecular pattern molecule, is significantly increased in COVID-19 patients and in the SARS-CoV-2-infected mice. Using IL-33-/- mice, we demonstrated that IL-33 deficiency is associated with significantly reduced bodyweight loss, tissue viral burdens, and lung pathology. This improved infection outcome in IL-33-/- mice correlated with reduced infiltrates of innate immune cells, i.e., neutrophils, macrophages, and natural killer cells, and activated T cells in inflamed lungs. Lung RNA-seq data revealed that IL-33 signaling enhances activation of inflammatory pathways, including interferon signaling, pathogen phagocytosis, macrophage activation and cytokine/chemokine. These findings unveil a pathogenic role of the alarmin IL-33 in SARS-CoV-2 infection, providing new insights that support the development of effective therapeutic strategies for COVID-19.
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