Table 1.
The paradox | Mouse | Human |
---|---|---|
Fibrosis and IBD | Fibrotic lesions such as those seen in CD are rarely observed in mouse models of IBD | Fibrosis and strictures are a common occurrence in CD |
IL-17 and IBD | IL-17 has been shown to be deleterious or protective | Antibody to IL-17 exacerbates inflammatory bowel disease |
Phenotype of immune cells | T cells from mice exposed to conventional microbiota resemble T cells from neonatal humans | Mature T cell phenotype in humans observed only in mice colonized with complex microbiota |
Clinical signs of infections | Mice fail to develop the clinical signs seen in humans after infection with H. pylori, C. difficile or influenza virus | H. pylori, C. difficile and influenza virus each produce a distinct disease in humans |
LPS | Mice relatively resistant to LPS | Humans very sensitive to LPS |
In these representative examples of differences between animal models and human disease, some heterogeneity could reflect technical limitations of genetic deletions that might not mimic specific alleles, whereas others might reflect environmental differences that affect microbiota or fundamental differences with evolutionary roots. H. pylori, Helicobacter pylori; C. difficile, Clostridium difficile; LPS, lipopolysaccharide.