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Updated: Jun 8, 2026
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Evaluating Therapeutic Interventions in the SHIP-deficient Mouse Model of Crohn Disease-like Ileitis and Fibrosis
Published on: October 14, 2025
SHIP deficiency causes Crohn's disease-like ileitis
William G Kerr1, Mi-Young Park, Monique Maubert
1SUNY Upstate Medical University, 750 E. Adams Street, 2204 Weiskotten Hall, Syracuse, NY 13210, USA. kerrw@upstate.edu
Gut
|October 14, 2010
Summary
The study reveals that SHIP deficiency causes inflammatory bowel disease (IBD) in mice, mimicking Crohn's disease. This immune dysfunction stems from altered T cell populations and increased neutrophils in the gut.
Area of Science:
- Immunology
- Gastroenterology
- Molecular Biology
Background:
- Inflammatory bowel disease (IBD) pathogenesis involves genetic factors affecting intestinal epithelial integrity and immune regulation.
- The SHIP protein is known to limit immunoregulatory cell numbers and function.
Purpose of the Study:
- To investigate the role of SHIP in maintaining immune tolerance within the gut mucosa.
- To determine if SHIP deficiency contributes to the development of IBD-like pathology.
Main Methods:
- Assessment of gastrointestinal pathology in SHIP-deficient and wild-type (WT) mice.
- Analysis of bone marrow chimeras involving WT and SHIP-deficient hematopoietic stem cells, splenocytes, T cells, and NK cells.
- Quantification of immune cell populations in the small intestine of SHIP-deficient and WT mice.
Main Results:
- SHIP-deficient mice exhibited segmental, transmural pyo-granulomatous ileitis, characteristic of Crohn's disease.
- Reconstitution of SHIP-deficient hosts with WT bone marrow corrected ileitis, while SHIP-deficient splenocytes transferred ileitis to WT hosts.
- SHIP deficiency led to a decrease in CD4 and CD8 T cells but a significant increase in neutrophils in the small intestine.
Conclusions:
- SHIP is crucial for intestinal immune function and its pathway warrants investigation in IBD patients.
- SHIP-deficient ileitis is proposed to result from impaired mucosal T cell immunity, leading to granulocyte-monocyte inflammation in the distal ileum.
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