Analysis Tools
digestive/alimentary system
| N |
• despite developing spontaneous ulcerative colitis, mice exhibit normal stomachs and small intestines
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• at 3.5 weeks, mice exhibit large epithelial discontinuities with a 4- to 5-fold increase in apoptosis of epithelial cells compared with wild-type or single homozygous mice
• however, treatment with anti-TNF-alpha antibodies normalizes the level of apoptosis
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• mice exhibit crypt loss associated with the development of colitis
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• mice exhibit anorectal prolapse unlike wild-type or single homozygous mice
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• at 3.5 weeks, colonic epithelial barrier is 2-fold more permeable than in Rag2tm1Fwa homozygotes
• at 4 to 5 weeks, colonic epithelial barrier is increased 3-fold
• at 5 to 6 weeks, colonic epithelial barrier is increased 8.6-fold
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• by 4 weeks, mice develop inflammation of the rectum and left colon unlike or single homozygous wild-type mice
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• mice exhibit inflammatory infiltrate in the lamina propria, neutrophil infiltration of the crypt and surface epithelium, and epithelial injury with surface denudations and ulcerations associated with crypt loss and epithelial mucodepletion
• by 4 weeks of age, mice develop highly penetrant and severe colitis unlike wild-type or single homozygous mice that increases in severity over time
• at 8 weeks, mice exhibit marked inflammation and colonic thickening unlike Rag2tm1Fwa homozygotes
• however, treatment with anti-TNF-alpha antibodies, T regulatory cells, or broad spectrum antibiotics restores normal colon phenotype, and treatment with broad spectrum antibiotics prevents communication of colitis to offspring
• female mice cross-fostering wild-type mice and Rag2tm1Fwa homozygotes fail to establish normal resistance to colitis in cross-fostered pups and mice can transmit susceptibility to colitis to wild-type mice housemates
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immune system
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• by 4 weeks, mice develop inflammation of the rectum and left colon unlike or single homozygous wild-type mice
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• mice exhibit inflammatory infiltrate in the lamina propria, neutrophil infiltration of the crypt and surface epithelium, and epithelial injury with surface denudations and ulcerations associated with crypt loss and epithelial mucodepletion
• by 4 weeks of age, mice develop highly penetrant and severe colitis unlike wild-type or single homozygous mice that increases in severity over time
• at 8 weeks, mice exhibit marked inflammation and colonic thickening unlike Rag2tm1Fwa homozygotes
• however, treatment with anti-TNF-alpha antibodies, T regulatory cells, or broad spectrum antibiotics restores normal colon phenotype, and treatment with broad spectrum antibiotics prevents communication of colitis to offspring
• female mice cross-fostering wild-type mice and Rag2tm1Fwa homozygotes fail to establish normal resistance to colitis in cross-fostered pups and mice can transmit susceptibility to colitis to wild-type mice housemates
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• as early as 2 weeks, colonic dendritic cells produce more TNF-alpha than wild-type cells
• in culture, bone marrow-derived dendritic cells produce more TNF-alpha compared with wild-type cells
• however, treatment with T regulatory cells reduced TNF-alpha levels
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endocrine/exocrine glands
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• mice exhibit crypt loss associated with the development of colitis
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Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| ulcerative colitis | DOID:8577 | J:141481 | ||
