ArticleAmerican journal of respiratory cell and molecular biology2014
Pivotal role of the 5-lipoxygenase pathway in lung injury after experimental sepsis.
Article in American journal of respiratory cell and molecular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 36 citations in OpenAlex.
- DPEP2 suppresses hyperinflammation via metabolic reprogramming of macrophages in sepsis.Nature communications · 2026Article
- Polyphenols mitigating inflammatory mechanisms in inflammatory bowel disease (IBD): focus on the NF-ƙB and JAK/STAT pathways.Inflammopharmacology · 2025Review
- Isoflurane attenuates sepsis-associated lung injury.Biochemical and biophysical research communications · 2022Article
- Respiratory Syncytial Virus Nonstructural Protein 1 Promotes 5-Lipoxygenase via miR-19a-3p.Journal of immunology research · 2022Article
- Formation, Signaling and Occurrence of Specialized Pro-Resolving Lipid Mediators-What is the Evidence so far?Frontiers in pharmacology · 2022Review
- Contributory Role of BLT2 in the Production of Proinflammatory Cytokines in Cecal Ligation and Puncture-Induced Sepsis.Molecules and cells · 2021Article
- Analysis of mRNA‑lncRNA and mRNA‑lncRNA-pathway co‑expression networks based on WGCNA in developing pediatric sepsis.Bioengineered · 2021Article
- Leukotrienes Are Dispensable for Vaginal Neutrophil Recruitment as Part of the Immunopathological Response During Experimental Vulvovaginal Candidiasis.Frontiers in microbiology · 2021Article
- A Novel Strategy to Mitigate the Hyperinflammatory Response to COVID-19 by Targeting Leukotrienes.Frontiers in pharmacology · 2020Article
- Paternal diet programs offspring health through sperm- and seminal plasma-specific pathways in mice.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Associations of the plasma lipidome with mortality in the acute respiratory distress syndrome: a longitudinal cohort study.Respiratory research · 2018Observational
- Identification of key pathogenic genes of sepsis based on the Gene Expression Omnibus database.Molecular medicine reports · 2018Article
- Too much of a good thing: How modulating LTBSeminars in immunology · 2017Review
- Invasive trophoblast promote stromal fibroblast decidualization via Profilin 1 and ALOX5.Scientific reports · 2017Article
- Pleiotropic regulations of neutrophil receptors response to sepsis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2017Review
- Opposing roles of LTB4 and PGE2 in regulating the inflammasome-dependent scorpion venom-induced mortality.Nature communications · 2016Article
- Article
- Myeloid derived hypoxia inducible factor 1-alpha is required for protection against pulmonary Aspergillus fumigatus infection.PLoS pathogens · 2014Article
- Article
- Cysteinyl leukotriene receptor-1 antagonists as modulators of innate immune cell function.Journal of immunology research · 2014Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
Postsepsis lung injury is a common clinical problem associated with significant morbidity and mortality. Leukotrienes (LTs) are important lipid mediators of infection and inflammation derived from the 5-lipoxygenase (5-LO) metabolism of arachidonate with the potential to contribute to lung damage after sepsis. To test the hypothesis that LTs are mediators of lung injury after sepsis, we assessed lung structure, inflammatory mediators, and mechanical changes after cecal ligation and puncture surgery in wild-type (WT) and 5-LO knockout (5-LO(-/-)) mice and in WT mice treated with a pharmacologic LT synthesis inhibitor (MK886) and LT receptor antagonists (CP105,696 and montelukast). Sixteen hours after surgery, WT animals exhibited severe lung injury (by histological analysis), substantial mechanical impairment (i.e., an increase in static lung elastance), an increase in neutrophil infiltration, and high levels of LTB4, cysteinyl-LTs (cys-LTs), prostaglandin E2, IL-1β, IL-6, IL-10, IL-17, KC (CXCL1), and monocyte chemotactic protein-1 (CCL2) in lung tissue and plasma. 5-LO(-/-) mice and WT mice treated with a pharmacologic 5-LO inhibitor were significantly protected from lung inflammation and injury. Selective antagonists for BLT1 or cys-LT1, the high-affinity receptors for LTB4 and cys-LTs, respectively, were insufficient to provide protection when used alone. These results point to an important role for 5-LO products in sepsis-induced lung injury and suggest that the use of 5-LO inhibitors may be of therapeutic benefit clinically.
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