ArticleJCI insight2018
Excessive localized leukotriene B4 levels dictate poor skin host defense in diabetic mice.
Article in JCI insight, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
31 citing papers in PubMed, 47 citations in OpenAlex.
- Plasma Resolvin D2 to Leukotriene BBioMed research international · 2021Trial
- Antimicrobial Peptides for Diabetic Foot Ulcers and Infections: Current Evidence and Translational Perspectives.International journal of molecular sciences · 2026Review
- Endogenous Lipid Signals in Energy Homeostasis and Fibrosis.Biomolecules · 2026Review
- Establishment of a murine resident dermal macrophage cell line.bioRxiv : the preprint server for biology · 2026Article
- PGEThe Journal of investigative dermatology · 2026Article
- Collagen binding adhesin restricts Staphylococcus aureus skin infection.Nature communications · 2026Article
- Marine bioactive peptides as potential therapeutic agents for wound healing - a review.Annals of medicine · 2025Review
- Scaffolds with spatiotemporally controlled growth factor delivery and cyclodextrin-enabled antagonism of growth factor receptor sequestration promote cutaneous wound healing.NPJ Regenerative medicine · 2025Article
- Metabolic Trajectories During Surgical Stress in Patients Undergoing Cardiac Surgery.bioRxiv : the preprint server for biology · 2025Article
- A CD4Immunity · 2025Article
- ATG5 suppresses type I IFN-dependent neutrophil effector functions during Mycobacterium tuberculosis infection in mice.Nature microbiology · 2025Article
- Metabolic pathways of eicosanoids-derivatives of arachidonic acid and their significance in skin.Cellular & molecular biology letters · 2025Review
- Exploring Skin Wound Healing Models and the Impact of Natural Lipids on the Healing Process.International journal of molecular sciences · 2024Review
- Molecular regulation of neutrophil swarming in health and disease: Lessons from the phagocyte oxidase.iScience · 2023Review
- Hyperglycemia Increases Severity of Staphylococcus aureus Osteomyelitis and Influences Bacterial Genes Required for Survival in Bone.Infection and immunity · 2023Article
- Quantitative Assessment of Low-Dose Photodynamic Therapy Effects on Diabetic Wound Healing Using Raman Spectroscopy.Pharmaceutics · 2023Article
- Leukotrienes in Innate Immunity: Still Underappreciated after All These Years?Journal of immunology (Baltimore, Md. : 1950) · 2023Review
- Acute Inflammation in Tissue Healing.International journal of molecular sciences · 2022Review
- Iron Dyshomeostasis in COVID-19: Biomarkers Reveal a Functional Link to 5-Lipoxygenase Activation.International journal of molecular sciences · 2022Article
- LTBDiabetes · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
Poorly controlled diabetes leads to comorbidities and enhanced susceptibility to infections. While the immune components involved in wound healing in diabetes have been studied, the components involved in susceptibility to skin infections remain unclear. Here, we examined the effects of the inflammatory lipid mediator leukotriene B4 (LTB4) signaling through its receptor B leukotriene receptor 1 (BLT1) in the progression of methicillin-resistant Staphylococcus aureus (MRSA) skin infection in 2 models of diabetes. Diabetic mice produced higher levels of LTB4 in the skin, which correlated with larger nonhealing lesion areas and increased bacterial loads compared with nondiabetic mice. High LTB4 levels were also associated with dysregulated cytokine and chemokine production, excessive neutrophil migration but impaired abscess formation, and uncontrolled collagen deposition. Both genetic deletion and topical pharmacological BLT1 antagonism restored inflammatory response and abscess formation, followed by a reduction in the bacterial load and lesion area in the diabetic mice. Macrophage depletion in diabetic mice limited LTB4 production and improved abscess architecture and skin host defense. These data demonstrate that exaggerated LTB4/BLT1 responses mediate a derailed inflammatory milieu that underlies poor host defense in diabetes. Prevention of LTB4 production/actions could provide a new therapeutic strategy to restore host defense in diabetes.
Indexed as
Identifiers
What Socratic holds
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 Socratic graph.