ArticleInflammatory bowel diseases2021
Human Intestinal Macrophages Are Involved in the Pathology of Both Ulcerative Colitis and Crohn Disease.
Article in Inflammatory bowel diseases, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers, 1 of them a synthesis that pooled it.
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Who cites it
107 citing papers in PubMed, 1 synthesis or guideline pooled it, 171 citations in OpenAlex.
- Preclinical studies of natural flavonoids in inflammatory bowel disease based on macrophages: a systematic review with meta-analysis and network pharmacology.Naunyn-Schmiedeberg's archives of pharmacology · 2025Pooled it
- The gut microbiota-tryptophan metabolism-immune axis in inflammatory bowel disease: Mechanisms and therapeutic prospects.Human vaccines & immunotherapeutics · 2026Review
- Systemic reprogramming of monocytes in Crohn's disease promotes their intestinal inflammatory function.JCI insight · 2026Article
- Regulation of Inducible Nitric Oxide Synthase (NOS2) Expression in Healthy and Inflamed Bowel: A Narrative Review.International journal of molecular sciences · 2026Review
- Identifying independent causal cell types for human diseases and risk variants.Cell genomics · 2026Article
- Article
- Red Ginseng Ethanolic Extract Alleviates DSS-Induced Colitis in Mice by Suppressing Inflammatory Mediator Production.International journal of molecular sciences · 2026Article
- TNIP3 Attenuates Colitis by Inhibiting the TAB1/NF-κB/NLRP3 Signaling Pathway in Macrophages.Digestive diseases and sciences · 2026Article
- Histone H3K27 demethylation drives Crohn's disease inflammation: GSK-J4 as a potential epigenetic therapy.Clinical epigenetics · 2026Article
- Transcriptional and ubiquitinative suppression of macrophage CST3 disrupts colonic homeostasis through defective efferocytosis.Cell death and differentiation · 2026Article
- METTL3/YTHDF1 drives M1 macrophage polarization and aggravates ulcerative colitis progression by regulating m6A modification of SerpinB5 mRNA and FBXO32-dependent NF-κB pathway.Journal of gastroenterology · 2026Article
- Dynamin-Related Protein 1 (Drp1) in Inflammatory Bowel Disease: Molecular Pathways Connecting Mitochondrial Dynamics with Intestinal Inflammation and Homeostasis.International journal of molecular sciences · 2026Review
- Structural Characterization and Anti-Colitis Mechanisms ofNutrients · 2026Article
- Surface hydrophobicity and rigidity determines protein corona on orally delivered nanoparticles treating colitis.Nature communications · 2026Article
- Myeloid Mcpip1/Regnase-1 regulates intestinal homeostasis by modulating epithelial cell differentiation.BMC gastroenterology · 2026Article
- Distinct transcriptional and epigenomic programs define Hofbauer cells in term placenta.JCI insight · 2026Article
- Generative AI-augmented transcriptomic and microbiome analysis across inflammatory and fibrotic disease states in Crohn's disease.Frontiers in artificial intelligence · 2026Article
- Intermittent fasting alleviates ulcerative colitis via lithocholic acid-mediated macrophage reprogramming.Frontiers in nutrition · 2026Article
- Macrophage dysregulation in inflammatory bowel disease: cellular heterogeneity, pathogenic mechanism, and treatment.Frontiers in immunology · 2026Review
- Acupoint Catgut Embedding Ameliorates Ulcerative Colitis in Association with Modulation of cGAS-STING Signaling and M1-Like/M2-Like Macrophage Markers.Journal of inflammation research · 2026Article
47 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundIntestinal macrophages are key immune cells in the maintenance of intestinal immune homeostasis and have a role in the pathogenesis of inflammatory bowel disease (IBD). However, the mechanisms by which macrophages exert a pathological influence in both ulcerative colitis (UC) and Crohn disease (CD) are not yet well understood.
methodsWe purified intestinal macrophages from gastrointestinal mucosal biopsies (patients with UC, patients with CD, and healthy donors) and analyzed their transcriptome by RNA sequencing and bioinformatics, confirming results with quantitative polymerase chain reaction and immunohistochemistry.
resultsCompared with those of healthy donors, intestinal macrophages in patients with UC and with CD showed cellular reprograming of 1287 and 840 dysregulated genes, respectively (false discovery rate ≤ 0.1). The UC and CD intestinal macrophages showed an activated M1 inflammatory phenotype and the downregulation of genes engaged in drug/xenobiotic metabolism. Only macrophages from CD showed, concomitant to an M1 phenotype, a significant enrichment in the expression of M2 and fibrotic and granuloma-related genes. For the first time, we showed (and validated by quantitative polymerase chain reaction and immunohistochemistry) that intestinal macrophages in patients with IBD present both M1 and M2 features, as recently described for tumor-associated macrophages, that affect key pathways for IBD pathology, represented by key markers such as MMP12 (fibrosis), CXCL9 (T-cell attraction), and CD40 (T-cell activation).
conclusionsOur data support the therapeutic targeting of macrophages to maintain remission in IBD but also indicate that a shift toward an M2 program-as proposed by some reports-may not limit the recruitment and activation of T cells because M2 features do not preclude M1 activation in patients with UC or CD and could exacerbate M2-related CD-specific features such as fibrosis and the formation of granulomas.
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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.