Table 1.

Commonly used animal models of intestinal fibrosis.

Designation	Descriptor	Technical Characteristics	Strengths and Drawbacks
DSS	Chemical	Repeated intermittent administration of DSS in the drinking water leads to inflammation and fibrosis Colonic localization	Simple and easily reproducible Model of epithelial injury and repair but not chronic inflammation Questionable relevance to IBD
TNBS	Chemical	Repeated intrarectal administration of TNBS/ethanol Colitis induction and severity may be unpredictable, depending on chemical batch and the animal strain Colonic localization	T-cell dependent mucosal injury at the colon Early/Th1 vs late/Th2-Th17 immunophenotype, which is compatible with the current paradigm for inflammation-induced fibrosis Pathological lesions include transmural inflammation Chemical injury/hapten utilization unrelated to IBD pathogenesis
PG-PS	Microbial	Subserosal injection of bacterial-derived PG-PS polymers in rats Cecal or small intestinal localization	Chronic granulomatous inflammation with significant fibrosis technically demanding artificial model
Fecal injection	Microbial	Intramural injection of filtered fecal suspension in rats Colonic localization	Focal colitis Transmural fibrosis with stricture formation Bacterial invasion may be relevant in IBD technically demanding
Salmonella Infection	Microbial	Pre-treatment with antibiotics, followed by ingestion of Salmonella Colonic localization	Infection with Salmonella in humans leads neither to chronic inflammation nor fibrosis
tgf-b1-Tg	Genetic	Overexpression of TGFβ via rectal instillation of an adenoviral vector, following ethanol-induced disruption of epithelial lining Colonic localization	Focal distribution of fibrosis Stricture formation TGFβ possibly relevant in IBD-associated fibrosis
tl1a-Tg	Genetic	Myeloid- or lymphoid-specific overexpression of TL1A Colonic and small intestinal localization	TL1A/DR3 is an important mucosal cytokine system Neutralization of TL1A exerts antifibrotic effect Fibrosis is affected by signals from the microbiota Mild inflammatory and fibrotic changes
mcp-1	Genetic	Intramural injection of an adenoviral vector carrying MCP-1 Colonic localization	TGFβ1 and collagen deposition Increase in collagen type 3:I ratio (similar to CD) Fibrosis is absent in RAG–/– mice Only MCP-1-dependent fibrogenesis is examined
SAMP1/Yit	Spontaneous	No chemical, immunological or genetic manipulation Small intestinal (terminal ileum) localization	Unbiased, spontaneous nature Pathology closely mimics Crohn’s disease Inflammation to fibrosis evolution traceable Precise immunopathogenetic mechanisms still unknown