ArticleJournal of Crohn's & colitis2016
Galectin-3 Plays an Important Pro-inflammatory Role in the Induction Phase of Acute Colitis by Promoting Activation of NLRP3 Inflammasome and Production of IL-1β in Macrophages.
Article in Journal of Crohn's & colitis, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.
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Who cites it
70 citing papers in PubMed, 129 citations in OpenAlex.
- Expression, Localization and Actions of Galectin-3: Implications in the Pathophysiology and Therapy of Cardiovascular Disease.International journal of molecular sciences · 2026Review
- Neurotrophins and Galectin-3: Hidden Keys in Neuroinflammation-A Narrative Review.International journal of molecular sciences · 2026Review
- Galectin-3 as a Key Driver of Neuroinflammation and α-Synuclein Aggregation in Parkinson's Disease: Unlocking New Paths for Biomarkers and Therapies.Cell biochemistry and biophysics · 2026Review
- Galectins: Role and Therapeutics in Diabetes and Diabetic Foot Ulcers.Biomolecules · 2026Review
- Altered distribution of tissue galectins correlates with mucosal dysregulation in SIV infection.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- When glycobiology meets inflammasome activation: Insights and implications.Journal of advanced research · 2026Review
- Diagnostic Potential of Periostin, Galectin-3 and Tenascin C Serum Measurements in Inflammatory Bowel Disease: Pilot Study.International journal of molecular sciences · 2025Article
- Interaction of potato-derived RG-I with galectin-3 and gene regulation in human mesenchymal stem cells.BMC biotechnology · 2025Article
- Review
- Glycosylation in neuroinflammation: mechanisms, implications, and therapeutic strategies for neurodegenerative diseases.Translational neurodegeneration · 2025Review
- Limiting endosomal damage sensing reduces inflammation triggered by lipid nanoparticle endosomal escape.Nature nanotechnology · 2025Article
- A Narrative Review on the Multifaceted Roles of Galectins in Host-Pathogen Interactions DuringInternational journal of molecular sciences · 2025Review
- Macrophage Signaling Pathways in Health and Disease: From Bench to Bedside Applications.MedComm · 2025Review
- Galectin-3-Insights from Inflammatory Bowel Disease and Primary Sclerosing Cholangitis.International journal of molecular sciences · 2025Review
- Proteomic analysis of hydrogen peroxide-treated human chondrocytes shows endoplasmic reticulum stress, cytoskeleton remodeling, and altered secretome composition.Cell communication and signaling : CCS · 2025Article
- Dichotomous effects of Galectin-9 in disease modulation in murine models of inflammatory bowel disease.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2025Article
- Galectin-3 disrupts tight junctions of airway epithelial cell monolayers by inducing expression and release of matrix metalloproteinases upon influenza A infection.Glycobiology · 2025Article
- The KLF4/Galectin-3 cascade is a key determinant of tubular cell death and acute kidney injury.International journal of biological sciences · 2025Article
- The importance of Galectin-3 in the diagnosis of childhood acute appendicitis.Turkish journal of medical sciences · 2025Article
- The interplay between hormonal vitamin D and lipopolysaccharide signaling on human neutrophil transcriptional responses.Frontiers in immunology · 2025Article
10 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND AND
aimsGalectin-3 [Gal-3] is an endogenous lectin with a broad spectrum of immunoregulatory effects: it plays an important role in autoimmune/inflammatory and malignant diseases, but the precise role of Gal-3 in pathogenesis of ulcerative colitis is still unknown.
methodsWe used a model of dextran sulphate sodium [DSS]-induced acute colitis. The role of Gal-3 in pathogenesis of this disease was tested by evaluating disease development in Gal-3 deficient mice and administration of Gal-3 inhibitor. Disease was monitored by clinical, histological, histochemical, and immunophenotypic investigations. Adoptive transfer was used to detect cellular events in pathogenesis.
resultsGenetic deletion or pharmacological inhibition of Gal-3 significantly attenuate DSS-induced colitis. Gal-3 deletion suppresses production of pro-inflammatory cytokines in colonic macrophages and favours their alternative activation, as well as significantly reducing activation of NOD-like receptor family, pyrin domain containing 3 [NLRP3] inflammasome in macrophages. Peritoneal macrophages isolated from untreated Gal-3(-/-) mice and treated in vitro with bacterial lipopolysaccharide or DSS produce lower amounts of tumour necrosis factor alpha [TNF-α] and interleukin beta [IL-1β] when compared with wild type [WT] cells. Genetic deletion of Gal-3 did not directly affect total neutrophils, inflammatory dendritic cells [DCs] or natural killer [NK] T cells. However, the total number of CD11c+ CD80+ DCs which produce pro-inflammatory cytokines, as well as TNF-α and IL-1β producing CD45+ CD11c- Ly6G+ neutrophils were significantly lower in colons of Gal-3(-/-) DSS-treated mice. Adoptive transfer of WT macrophages significantly enhanced the severity of disease in Gal-3(-/-) mice.
conclusionsGal-3 expression promotes acute DSS-induced colitis and plays an important pro-inflammatory role in the induction phase of colitis by promoting the activation of NLRP3 inflammasome and production of IL-1β in macrophages.
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