ArticleScience signaling2015
Leukotriene B4-mediated sterile inflammation promotes susceptibility to sepsis in a mouse model of type 1 diabetes.
Article in Science signaling, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 63 citations in OpenAlex.
- Establishment of a murine resident dermal macrophage cell line.bioRxiv : the preprint server for biology · 2026Article
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- High glucose heightens vulnerability toEmerging microbes & infections · 2025Article
- The Role ofBiomolecules · 2025Review
- Proarrhythmic Lipid Inflammatory Mediators: Mechanisms in Obesity Arrhythmias.Journal of cellular physiology · 2025Review
- Advances in the Regulation of Inflammatory Mediators in Nitric Oxide Synthase: Implications for Disease Modulation and Therapeutic Approaches.International journal of molecular sciences · 2025Review
- Inhibition of Leukotriene ACartilage · 2024Article
- The role of captopril in leukotriene deficient type 1 diabetic mice.Scientific reports · 2023Article
- Exosomal non coding RNAs as a novel target for diabetes mellitus and its complications.Non-coding RNA research · 2023Review
- Hyperglycemia Increases Severity of Staphylococcus aureus Osteomyelitis and Influences Bacterial Genes Required for Survival in Bone.Infection and immunity · 2023Article
- Functions and mechanisms of cytosolic phospholipase ANeural regeneration research · 2023Review
- Leukotrienes in Innate Immunity: Still Underappreciated after All These Years?Journal of immunology (Baltimore, Md. : 1950) · 2023Review
- Extracellular vesicles in β cell biology: Role of lipids in vesicle biogenesis, cargo, and intercellular signaling.Molecular metabolism · 2022Review
- The anti-inflammatory and antioxidant effects of Montelukast on lung sepsis in adult mice.Journal of medicine and life · 2022Article
- Effect of Dysglycemia on Urinary Lipid Mediator Profiles in Persons With Pulmonary Tuberculosis.Frontiers in immunology · 2022Observational
- LTBDiabetes · 2021Article
- SOCS-1 inhibition of type I interferon restrains Staphylococcus aureus skin host defense.PLoS pathogens · 2021Article
- Unbalanced production of LTBEmerging microbes & infections · 2020Article
- Leukotriene BProceedings of the National Academy of Sciences of the United States of America · 2020Article
- Lipid mediators of inflammation and Resolution in individuals with tuberculosis and tuberculosis-Diabetes.Prostaglandins & other lipid mediators · 2020Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Type 1 diabetes mellitus (T1DM) is associated with chronic systemic inflammation and enhanced susceptibility to systemic bacterial infection (sepsis). We hypothesized that low insulin concentrations in T1DM trigger the enzyme 5-lipoxygenase (5-LO) to produce the lipid mediator leukotriene B4 (LTB4), which triggers systemic inflammation that may increase susceptibility to polymicrobial sepsis. Consistent with chronic inflammation, peritoneal macrophages from two mouse models of T1DM had greater abundance of the adaptor MyD88 (myeloid differentiation factor 88) and its direct transcriptional effector STAT-1 (signal transducer and activator of transcription 1) than macrophages from nondiabetic mice. Expression of Alox5, which encodes 5-LO, and the concentration of the proinflammatory cytokine interleukin-1β (IL-1β) were also increased in peritoneal macrophages and serum from T1DM mice. Insulin treatment reduced LTB4 concentrations in the circulation and Myd88 and Stat1 expression in the macrophages from T1DM mice. T1DM mice treated with a 5-LO inhibitor had reduced Myd88 mRNA in macrophages and increased abundance of IL-1 receptor antagonist and reduced production of IL-β in the circulation. T1DM mice lacking 5-LO or the receptor for LTB4 also produced less proinflammatory cytokines. Compared to wild-type or untreated diabetic mice, T1DM mice lacking the receptor for LTB4 or treated with a 5-LO inhibitor survived polymicrobial sepsis, had reduced production of proinflammatory cytokines, and had decreased bacterial counts. These results uncover a role for LTB4 in promoting sterile inflammation in diabetes and the enhanced susceptibility to sepsis in T1DM.
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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.