ArticleProceedings of the National Academy of Sciences of the United States of America2004
Identification of hepoxilin A3 in inflammatory events: a required role in neutrophil migration across intestinal epithelia.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 100 papers, 1 of them a synthesis that pooled it.
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
100 citing papers in PubMed, 1 synthesis or guideline pooled it, 170 citations in OpenAlex.
- Identifying serum metabolite biomarkers for autoimmune diseases: a two-sample mendelian randomization and meta-analysis.Frontiers in immunology · 2024Pooled it
- Hepoxilin A(3) facilitates neutrophilic breach of lipoxygenase-expressing airway epithelial barriers.Journal of immunology (Baltimore, Md. : 1950) · 2012Trial
- Transient receptor potential vanilloid 2 functions as a directional driver for hepoxilin AScience advances · 2026Article
- Review
- Mechanisms conferring multi-layered protection against intestinal Salmonella Typhimurium infection.FEMS microbiology reviews · 2025Review
- Oxidized phospholipid and transcriptomic signatures of THC-related vaping associated lung injury.Scientific reports · 2024Article
- Blocking HXAmBio · 2024Article
- Causality of genetically determined blood metabolites on inflammatory bowel disease: a two-sample Mendelian randomization study.Scientific reports · 2024Article
- Fungal melanin suppresses airway epithelial chemokine secretion through blockade of calcium fluxing.Nature communications · 2024Article
- Blocking HXAbioRxiv : the preprint server for biology · 2024Article
- Article
- Phenotypic and Functional Diversity of Neutrophils in Gut Inflammation and Cancer.The American journal of pathology · 2024Review
- Review
- The role of selenoproteins in neutrophils during inflammation.Archives of biochemistry and biophysics · 2022Article
- Uncovering mechanisms of brain inflammation in Alzheimer's disease with APOE4: Application of single cell-type lipidomics.Annals of the New York Academy of Sciences · 2022Review
- Baseline Elevations of Leukotriene Metabolites and Altered Plasmalogens Are Prognostic Biomarkers of Plaque Progression in Systemic Lupus Erythematosus.Frontiers in cardiovascular medicine · 2022Article
- SepA EnhancesmBio · 2021Article
- Dichotomous roles of neutrophils in modulating pathogenic and repair processes of inflammatory bowel diseases.Precision clinical medicine · 2021Review
- Regulation of Tissue Inflammation by 12-Lipoxygenases.Biomolecules · 2021Review
- Regulatory mechanisms of neutrophil migration from the circulation to the airspace.Cellular and molecular life sciences : CMLS · 2021Review
40 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
The mechanism by which neutrophils [polymorphonuclear leukocyte (PMNs)] are stimulated to move across epithelial barriers at mucosal surfaces has been basically unknown in biology. IL-8 has been shown to stimulate PMNs to leave the bloodstream at a local site of mucosal inflammation, but the chemical gradient used by PMNs to move between adjacent epithelial cells and traverse the tight junction at the apical neck of these mucosal barriers has eluded identification. Our studies not only identify this factor, previously termed pathogen-elicited epithelial chemoattractant, as the eicosanoid hepoxilin A(3) (hepA(3)) but also demonstrate that it is a key factor promoting the final step in PMN recruitment to sites of mucosal inflammation. We show that hepA(3) is synthesized by epithelial cells and secreted from their apical surface in response to conditions that stimulate inflammatory events. Our data further establish that hepA(3) acts to draw PMNs, via the establishment of a gradient across the epithelial tight junction complex. The functional significance of hepA(3) to target PMNs to the lumen of the gut at sites of inflammation was demonstrated by the finding that disruption of the 12-lipoxygenase pathway (required for hepA(3) production) could dramatically reduce PMN-mediated tissue trauma, demonstrating that hepA(3) is a key regulator of mucosal inflammation.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.