ArticleThe American journal of pathology2011
SHIP-deficient mice develop spontaneous intestinal inflammation and arginase-dependent fibrosis.
Article in The American journal of pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 50 citations in OpenAlex.
- Mast cell-derived IL-13 as a driver of Crohn disease-associated intestinal fibrosis.Inflammatory bowel diseases · 2026Article
- Insights into the Molecular Mechanisms and Novel Therapeutic Strategies of Stenosis Fibrosis in Crohn's Disease.Biomedicines · 2025Review
- Hongyuyin attenuates intestinal fibrosis in ulcerative colitis in mice revealed by transcriptomic and network pharmacology analyses.Scientific reports · 2025Article
- NLRP3: a key regulator of skin wound healing and macrophage-fibroblast interactions in mice.Cell communication and signaling : CCS · 2025Article
- Environmental and inflammatory factors influencing concurrent gut and lung inflammation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024Article
- Colonic Tuft Cells: The Less-Recognized Therapeutic Targets in Inflammatory Bowel Disease and Colorectal Cancer.International journal of molecular sciences · 2024Review
- Establishment of persistent enteric mycobacterial infection following streptomycin pre-treatment.Gut pathogens · 2023Article
- Regulation of Microglial Signaling by Lyn and SHIP-1 in the Steady-State Adult Mouse Brain.Cells · 2023Article
- Regulation of microglial responses after pediatric traumatic brain injury: exploring the role of SHIP-1.Frontiers in neuroscience · 2023Article
- Harnessing murine models of Crohn's disease ileitis to advance concepts of pathophysiology and treatment.Mucosal immunology · 2022Review
- Myeloid arginase-1 controls excessive inflammation and modulates T cell responses in Pseudomonas aeruginosa pneumonia.Immunobiology · 2021Article
- Selective inhibition of arginase-2 in endothelial cells but not proximal tubules reduces renal fibrosis.JCI insight · 2020Article
- Phosphatidylinositol 3-kinase p110δ drives intestinal fibrosis in SHIP deficiency.Mucosal immunology · 2019Article
- Inhibition of chlorine-induced airway fibrosis by budesonide.Toxicology and applied pharmacology · 2019Article
- Compositional changes to the ileal microbiome precede the onset of spontaneous ileitis in SHIP deficient mice.Gut microbes · 2019Article
- AQX-1125, small molecule SHIP1 activator inhibits bleomycin-induced pulmonary fibrosis.British journal of pharmacology · 2017Article
- Article
- Bifidobacterium breve reduces apoptotic epithelial cell shedding in an exopolysaccharide and MyD88-dependent manner.Open biology · 2017Article
- Bidirectional crosstalk via IL-6, PGE2 and PGD2 between murine myofibroblasts and alternatively activated macrophages enhances anti-inflammatory phenotype in both cells.British journal of pharmacology · 2016Article
- Expression of arginase I and inducible nitric oxide synthase in the peripheral blood and lymph nodes of HIV‑positive patients.Molecular medicine reports · 2016Article
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Authors and funding
9 authors at 3 institutions in 3 countries.
Funding
Abstract
Intestinal fibrosis is a serious complication of Crohn's disease (CD) that can lead to stricture formation, which requires surgery. Mechanisms underlying intestinal fibrosis remain elusive because of a lack of suitable mouse models. Herein, we describe a spontaneous mouse model of intestinal inflammation with fibrosis and the profibrotic role of arginase I. The Src homology 2 domain-containing inositol polyphosphate 5'-phosphatase-deficient (SHIP(-/-)) mice developed spontaneous discontinuous intestinal inflammation restricted to the distal ileum starting at the age of 4 weeks. Mice developed several key features resembling CD, including inflammation and fibrosis. Inflammation was characterized by abundant infiltrating Gr-1-positive immune cells, granuloma-like immune cell aggregates that contained multinucleated giant cells, and a mixed type 2 and type 17 helper T-cell cytokine profile. Fibrosis was characterized by a thickened ileal muscle layer, collagen deposition, and increased fibroblasts at the sites of collagen deposition. SHIP(-/-) ilea had increased arginase activity and arginase I expression that was inversely proportional to nitrotyrosine staining. SHIP(-/-) mice were treated with the arginase inhibitor S-(2-boronoethyl)-l-cysteine, and changes in the disease phenotype were measured. Arginase inhibition did not affect the number of immune cell infiltrates in the SHIP(-/-) mouse ilea; rather, it reduced collagen deposition and muscle hyperplasia. These findings suggest that arginase activity is a potential target to limit intestinal fibrosis in patients with CD.
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