ArticleClinical and experimental immunology2013
Expression of Toll-like receptor-3 is enhanced in active inflammatory bowel disease and mediates the excessive release of lipocalin 2.
Article in Clinical and experimental immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 53 citations in OpenAlex.
- Safety and tolerability of anti-toll-like receptor 3, monoclonal antibody PRV-300 in patients with moderate-to-severe ulcerative colitis: a randomized phase 1B clinical trial (PULSE).Journal of Crohn's & colitis · 2026Trial
- Lactobacillus brevis cell-free supernatant attenuates inflammation-associated gene expression and differentially modulates host defense-associated genes in DSS-stimulated HT-29 cells.Molecular biology reports · 2026Article
- Clinical Value of Neutrophil Gelatinase-Associated Lipocalin as a Non-Invasive Biomarker for Intestinal Ulcer in Behçet's Syndrome: A Pilot Study.International journal of molecular sciences · 2026Article
- The Roles of Four Neutrophil-Derived Proteins as Non-Invasive Biomarkers in the Assessment of Inflammatory Bowel Disease.Journal of inflammation research · 2026Review
- Single cell transcriptional analysis of human adenoids identifies molecular features of airway microfold cells.Mucosal immunology · 2025Article
- Sex- and site-specific associations of circulating lipocalin 2 and incident colorectal cancer: Results from the EPIC cohort.International journal of cancer · 2025Article
- The dietary phytochemicals carnosic acid and sulforaphane regulate inflammatory markers in ulcerative colitis patient-derived colonoids.Frontiers in pharmacology · 2025Article
- Inflammation, Autoinflammation and Autoimmunity in Inflammatory Bowel Diseases.Current issues in molecular biology · 2023Review
- Physiological hypoxia improves growth and functional differentiation of human intestinal epithelial organoids.Frontiers in immunology · 2023Article
- Lipocalin 2 activates the NLRP3 inflammasome via LPS‑induced NF‑κB signaling and plays a role as a pro‑inflammatory regulator in murine macrophages.Molecular medicine reports · 2022Article
- Mucosal gene expression profile of stricturing Crohn's disease: A preliminary study.Experimental and therapeutic medicine · 2022Article
- DSS-induced inflammation in the colon drives a proinflammatory signature in the brain that is ameliorated by prophylactic treatment with the S100A9 inhibitor paquinimod.Journal of neuroinflammation · 2021Article
- Host-Viral Interactions in the Pathogenesis of Ulcerative Colitis.International journal of molecular sciences · 2021Review
- Mucosal and faecal neutrophil gelatinase-associated lipocalin as potential biomarkers for collagenous colitis.Journal of gastroenterology · 2021Article
- Integrated Analysis of Multiple Microarray Studies to Identify Novel Gene Signatures in Ulcerative Colitis.Frontiers in genetics · 2021Article
- Review
- Lipocalin-2 is dispensable in inflammation-induced sickness and depression-like behavior.Psychopharmacology · 2019Article
- Functions and regulation of lipocalin-2 in gut-origin sepsis: a narrative review.Critical care (London, England) · 2019Review
- Ulcer-associated cell lineage expresses genes involved in regeneration and is hallmarked by high neutrophil gelatinase-associated lipocalin (NGAL) levels.The Journal of pathology · 2019Article
- Lipocalin 24p3 Induction in Colitis Adversely Affects Inflammation and Contributes to Mortality.Frontiers in immunology · 2019Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Anti-microbial peptides might influence the pathogenesis and course of inflammatory bowel disease (IBD). We sought to clarify the role of the anti-microbial glycoprotein lipocalin 2 (LCN2) in the colon by determining its localization and regulation in IBD. Following a microarray gene expression study of colonic biopsies from a large IBD population (n = 133), LCN2 was localized using immunohistochemistry and in-situ hybridization. Moreover, we examined the regulation of LCN2 in HT-29 cells with a panel of pattern recognition receptors (PRRs) and sought evidence by immunohistochemistry that the most relevant PRR, the Toll-like receptor (TLR)-3, was indeed expressed in colonic epithelium in IBD. LCN2 was among the 10 most up-regulated genes in both active ulcerative colitis (UCa) and active Crohn's disease (CDa) versus healthy controls. LCN2 protein was found in both epithelial cells and infiltrating neutrophils, while mRNA synthesis was located solely to epithelial cells, indicating that de-novo synthesis and thus regulation of LCN2 as measured in the gene expression analysis takes place in the mucosal epithelial cells. LCN2 is a putative biomarker in faeces for intestinal inflammation, different from calprotectin due to its epithelial site of synthesis. LCN2 release from the colonic epithelial cell line HT-29 was enhanced by both interleukin (IL)-1β and the TLR-3 ligand poly(I:C), and TLR-3 was shown to be expressed constitutively in colonic epithelial cells and markedly increased during inflammation.
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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.