ArticleJournal of molecular cell biology2023
SARS-CoV-2 spike protein as a bacterial lipopolysaccharide delivery system in an overzealous inflammatory cascade.
Article in Journal of molecular cell biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
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Who cites it
14 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Efficacy and safety of glycyrrhizic acid preparation treating comorbid liver injury in COVID-19: A systematic review.Frontiers in pharmacology · 2022Pooled it
- Pathogen-Specific Regulation of Renin-Angiotensin System Genes in Epithelial Cells: A Comparative Study of SARS-CoV-2 Spike Protein N-Terminal Domain Fragment and Bacterial Lipopolysaccharide.Pathogens (Basel, Switzerland) · 2026Article
- Etiology Model of Kawasaki Disease and Multisystem Inflammatory Syndromes: Mast Cell Activation.Current issues in molecular biology · 2026Article
- Conservation of Bacterial Lipopolysaccharide Binding by SARS-CoV-2 Spike across Major Viral Variants.Computational and structural biotechnology journal · 2026Article
- Oral SARS-CoV-2 Infection and Risk for Long Covid.Reviews in medical virology · 2025Review
- Intestinal barrier compromise, viral persistence, and immune dysregulation converge on neurological sequelae in Long COVID.Frontiers in aging neuroscience · 2025Review
- The innate immune response in SARS-CoV2 infection: focus on toll-like receptor 4 in severe disease outcomes.Frontiers in immunology · 2025Review
- Vaccination and COVID-19: impact on long-COVID.Frontiers in immunology · 2025Review
- Risk factors for severe COVID-19 disease increase SARS-CoV-2 infectivity of endothelial cells and pericytes.Open biology · 2024Article
- Review
- Article
- Endotoxin tolerance and low activation of TLR-4/NF-κB axis in monocytes of COVID-19 patients.Journal of molecular medicine (Berlin, Germany) · 2023Article
- Growth hormone-releasing hormone antagonist MIA-602 inhibits inflammation induced by SARS-CoV-2 spike protein and bacterial lipopolysaccharide synergism in macrophages and human peripheral blood mononuclear cells.Frontiers in immunology · 2023Article
- SARS-CoV-2 spike protein aggregation is triggered by bacterial lipopolysaccharide.FEBS letters · 2022Article
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Accumulating evidence indicates a potential role for bacterial lipopolysaccharide (LPS) in the overactivation of the immune response during SARS-CoV-2 infection. LPS is recognized by Toll-like receptor 4, mediating proinflammatory effects. We previously reported that LPS directly interacts with SARS-CoV-2 spike (S) protein and enhances proinflammatory activities. Using native gel electrophoresis and hydrogen-deuterium exchange mass spectrometry, we showed that LPS binds to multiple hydrophobic pockets spanning both the S1 and S2 subunits of the S protein. Molecular simulations validated by a microscale thermophoresis binding assay revealed that LPS binds to the S2 pocket with a lower affinity compared to S1, suggesting a role as an intermediate in LPS transfer. Congruently, nuclear factor-kappa B (NF-κB) activation in monocytic THP-1 cells is strongly boosted by S2. Using NF-κB reporter mice followed by bioimaging, a boosting effect was observed for both S1 and S2, with the former potentially facilitated by proteolysis. The Omicron S variant binds to LPS, but with reduced affinity and LPS boosting in vitro and in vivo. Taken together, the data provide a molecular mechanism by which S protein augments LPS-mediated hyperinflammation.
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Registered trials
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