ReviewThe Journal of biological chemistry2019
Phospholipid regulation of innate immunity and respiratory viral infection.
Review in The Journal of biological chemistry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
45 citing papers in PubMed, 89 citations in OpenAlex.
- Integrated Metabolomics and Network Pharmacology to Reveal the Mechanisms ofInternational journal of molecular sciences · 2025Article
- Review
- The Therapeutic Potential of Myo-Inositol in Managing Patients with Respiratory Diseases.International journal of molecular sciences · 2025Review
- The innate immune response in SARS-CoV2 infection: focus on toll-like receptor 4 in severe disease outcomes.Frontiers in immunology · 2025Review
- A therapy for suppressing canonical and noncanonical SARS-CoV-2 viral entry and an intrinsic intrapulmonary inflammatory response.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Interplay of TLR4 and SARS-CoV-2: Unveiling the Complex Mechanisms of Inflammation and Severity in COVID-19 Infections.Journal of inflammation research · 2024Review
- TLR4 signalling: the key to controlling EV71 replication and inflammatory response.Frontiers in cellular and infection microbiology · 2024Article
- Therapeutic benefits of glycerol in dry eye disease.Frontiers in medicine · 2024Article
- Network pharmacology combined with metabolomics to explore the mechanism for Lonicerae Japonicae flos against respiratory syncytial virus.BMC complementary medicine and therapies · 2023Article
- Surfactant replacement therapy as promising treatment for COVID-19: an updated narrative review.Bioscience reports · 2023Review
- Immune response in influenza virus infection and modulation of immune injury by viral neuraminidase.Virology journal · 2023Review
- The anti-inflammatory and antiviral properties of anionic pulmonary surfactant phospholipids.Immunological reviews · 2023Review
- Anionic Pulmonary Surfactant Lipid Treatment Inhibits Rhinovirus A Infection of the Human Airway Epithelium.Viruses · 2023Article
- The Role of Pulmonary Surfactant Phospholipids in Fibrotic Lung Diseases.International journal of molecular sciences · 2022Review
- Innate Immune System Activation, Inflammation and Corneal Wound Healing.International journal of molecular sciences · 2022Review
- Fumonisin B Series Mycotoxins' Dose Dependent Effects on the Porcine Hepatic and Pulmonary Phospholipidome.Toxins · 2022Article
- Article
- Reprogrammed Lipid Metabolism and the Lipid-Associated Hallmarks of Colorectal Cancer.Cancers · 2022Review
- PGE2 inhibits neutrophil phagocytosis through the EP2R-cAMP-PTEN pathway.Immunity, inflammation and disease · 2022Article
- A novel non-invasive method allowing for discovery of pathologically relevant proteins from small airways.Clinical proteomics · 2022Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Toll-like receptors (TLRs) coupled to intracellular signaling cascades function as central elements of innate immunity that control transcription of numerous pro-inflammatory genes. Two minor anionic phospholipids present in the pulmonary surfactant complex, palmitoyl-oleoyl-phosphatidylglycerol (POPG) and phosphatidylinositol (PI), antagonize the cognate ligand activation of TLRs 2 and 4. The lipids block recognition of activating ligands by the TLRs, either directly or via the TLR4 coreceptors CD14 and MD2. Antagonism of TLR activation results in inhibition of the initiating step of the pro-inflammatory signaling pathways. Evidence for this mechanism of action comes from direct binding studies between CD14 and MD2 with POPG and PI. Additional evidence for this mechanism of antagonism also comes from monitoring the reduction of protein phosphorylation events that characterize the intracellular signaling by activated TLRs. The pathogenesis of respiratory syncytial virus (RSV) and influenza A virus (IAV) have been linked to TLR4 activation, and we examined the action of POPG and PI as potential antagonists of the pathology of these viruses. Surprisingly, POPG and PI dramatically curtail infection, in addition to inhibiting inflammatory sequelae associated with RSV and IAV infections. The mechanism of action by the lipids is disruption of virus particle binding to host cell plasma membrane receptors, required for viral uptake. The antagonism of activation of TLRs and virus binding to the alveolar epithelium by resident constituents of the pulmonary surfactant system suggests that POPG and PI function in homeostasis, to prevent inflammatory processes that result in reductions in gas exchange within the alveolar compartment.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.