ArticleInfection and immunity2011
LOX-1 deletion improves neutrophil responses, enhances bacterial clearance, and reduces lung injury in a murine polymicrobial sepsis model.
Article in Infection and immunity, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 72 citations in OpenAlex.
- Culturing neutrophils from human CD34STAR protocols · 2026Article
- Early soluble LOX-1, cerebral perfusion, and intrauterine inflammation in very and extremely preterm infants.Pediatric research · 2026Observational
- Oxidation of low-density lipoprotein by hemoglobin causes pulmonary microvascular endothelial barrier dysfunction through lectin-like oxidized LDL receptor 1.American journal of physiology. Lung cellular and molecular physiology · 2025Article
- Elevated plasma soluble lectin-like oxidised low-density lipoprotein receptor 1 as an independent prognostic biomarker in sepsis.Lipids in health and disease · 2025Article
- Increased circulating LOX-1Heliyon · 2024Article
- Sepsis in elderly patients: the role of neutrophils in pathophysiology and therapy.Internal and emergency medicine · 2024Review
- New insight into arginine and tryptophan metabolism in macrophage activation during tuberculosis.Frontiers in immunology · 2024Review
- Detailed phenotyping reveals diverse and highly skewed neutrophil subsets in both the blood and airways during active tuberculosis infection.Frontiers in immunology · 2024Article
- Review
- Innate immune responses in pneumonia.Pneumonia (Nathan Qld.) · 2023Review
- Lectin-like oxidized low-density lipoprotein receptor 1 attenuates pneumonia-induced lung injury.JCI insight · 2022Article
- The Impact of Cytokines on Neutrophils' Phagocytosis and NET Formation during Sepsis-A Review.International journal of molecular sciences · 2022Review
- Knockdown of lectin-like oxidized low-density lipoprotein-1 ameliorates alcoholic cardiomyopathy via inactivating the p38 mitogen-activated protein kinase pathway.Bioengineered · 2022Article
- Lectin-type oxidized LDL receptor 1 modulates matrix metalloproteinase 2 production in peri-implantitis.Experimental and therapeutic medicine · 2022Article
- The amniotic fluid proteome changes with gestational age in normal pregnancy: a cross-sectional study.Scientific reports · 2022Article
- Scavenger receptors in host defense: from functional aspects to mode of action.Cell communication and signaling : CCS · 2022Review
- Critical role of oxidized LDL receptor-1 in intravascular thrombosis in a severe influenza mouse model.Scientific reports · 2021Article
- Lipid and Lipoprotein Dysregulation in Sepsis: Clinical and Mechanistic Insights into Chronic Critical Illness.Journal of clinical medicine · 2021Review
- LOX-1-Expressing Immature Neutrophils Identify Critically-Ill COVID-19 Patients at Risk of Thrombotic Complications.Frontiers in immunology · 2021Article
- Using RNA-Seq to Investigate Immune-Metabolism Features in Immunocompromised Patients With Sepsis.Frontiers in medicine · 2021Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Inflammatory tissue injury and immunosuppression are the major causes of death in sepsis. Novel therapeutic targets that can prevent excessive inflammation and improve immune responses during sepsis could be critical for treatment of this devastating disease. LOX-1 (lectin-like oxidized low-density lipoprotein receptor-1), a membrane protein expressed in endothelial cells, has been known to mediate vascular inflammation. In the present study, we demonstrated that LOX-1 deletion markedly improved the survival rate in a murine model of polymicrobial sepsis. Wild-type (LOX-1(+/+)) and LOX-1 knockout (LOX-1(-/-)) mice were subjected to cecal ligation and puncture (CLP) to induce sepsis. LOX-1 deletion significantly reduced systemic inflammation and inflammatory lung injury during sepsis, together with decreased production of proinflammatory cytokines and reduced lung edema formation. Furthermore, LOX-1 deletion improved host immune responses after the induction of sepsis, as indicated by enhanced bacterial clearance. Interestingly, we were able to demonstrate that LOX-1 is expressed in neutrophils. LOX-1 deletion prevented neutrophil overreaction and increased neutrophil recruitment to infection sites after sepsis induction, contributing at least partly to increased immune responses in LOX-1 knockout mice. Our study results indicate that LOX-1 is an important mediator of inflammation and neutrophil dysfunction in sepsis.
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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.