Genetic Factors in Animal Models of Intestinal Inflammation
The critical importance of host genetic susceptibility in determining chronicity, aggressiveness and complications of intestinal inflammation is clearly demonstrated by studies of inbred rodents, transgenic rats and spontaneous mutants. Inbred Lewis rats challenged by purified bacterial cell wall po...
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| Format: | Article |
| Language: | English |
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Wiley
1995-01-01
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| Series: | Canadian Journal of Gastroenterology |
| Online Access: | http://dx.doi.org/10.1155/1995/604564 |
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| author | R Balfour Sartor |
| author_facet | R Balfour Sartor |
| author_sort | R Balfour Sartor |
| collection | DOAJ |
| description | The critical importance of host genetic susceptibility in determining chronicity, aggressiveness and complications of intestinal inflammation is clearly demonstrated by studies of inbred rodents, transgenic rats and spontaneous mutants. Inbred Lewis rats challenged by purified bacterial cell wall polymers, indomethacin or small bowel bacterial overgrowth develop chronic granulomatous intestinal inflammation with fibrosis and extraintestinal manifestations, whereas Fischer (major histocompatibility complex identical to Lewis) and Buffalo rats identically stimulated demonstrate only self-limited enterocolitis with no chronic inflammation, fibrosis, granulomas or extraintestinal inflammation. Similar differential patterns of intestinal inflammation are apparent in inbred mouse strains challenged with trinitrobenzene-sulphonic acid, Citrobacter freundii or backcrossed with T cell receptor deficient (knockout) mice. The dominant role of genetic background in induction of intestinal inflammation is further documented by spontaneous colitis which develops in spontaneously mutant mice, cotton-top tamarins, human leukocyte antigen-B27/ β2 microglobulin transgenic rats and mice with targeted deletions of certain immunoregulatory cytokine and T lymphocyte genes. Identification of the immunological mechanisms of host genetic susceptibility and the genetic basis of spontaneous colitis should provide new insights into the pathogenesis of human inflammatory bowel disease. |
| format | Article |
| id | doaj-art-d3f74378254d421a9efae98a020fe3d8 |
| institution | Kabale University |
| issn | 0835-7900 |
| language | English |
| publishDate | 1995-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Canadian Journal of Gastroenterology |
| spelling | doaj-art-d3f74378254d421a9efae98a020fe3d82025-02-03T05:58:57ZengWileyCanadian Journal of Gastroenterology0835-79001995-01-019314715210.1155/1995/604564Genetic Factors in Animal Models of Intestinal InflammationR Balfour Sartor0Center for Gastrointestinal Biology and Disease, University of North Carolina, Chapel Hill, North Carolina, USAThe critical importance of host genetic susceptibility in determining chronicity, aggressiveness and complications of intestinal inflammation is clearly demonstrated by studies of inbred rodents, transgenic rats and spontaneous mutants. Inbred Lewis rats challenged by purified bacterial cell wall polymers, indomethacin or small bowel bacterial overgrowth develop chronic granulomatous intestinal inflammation with fibrosis and extraintestinal manifestations, whereas Fischer (major histocompatibility complex identical to Lewis) and Buffalo rats identically stimulated demonstrate only self-limited enterocolitis with no chronic inflammation, fibrosis, granulomas or extraintestinal inflammation. Similar differential patterns of intestinal inflammation are apparent in inbred mouse strains challenged with trinitrobenzene-sulphonic acid, Citrobacter freundii or backcrossed with T cell receptor deficient (knockout) mice. The dominant role of genetic background in induction of intestinal inflammation is further documented by spontaneous colitis which develops in spontaneously mutant mice, cotton-top tamarins, human leukocyte antigen-B27/ β2 microglobulin transgenic rats and mice with targeted deletions of certain immunoregulatory cytokine and T lymphocyte genes. Identification of the immunological mechanisms of host genetic susceptibility and the genetic basis of spontaneous colitis should provide new insights into the pathogenesis of human inflammatory bowel disease.http://dx.doi.org/10.1155/1995/604564 |
| spellingShingle | R Balfour Sartor Genetic Factors in Animal Models of Intestinal Inflammation Canadian Journal of Gastroenterology |
| title | Genetic Factors in Animal Models of Intestinal Inflammation |
| title_full | Genetic Factors in Animal Models of Intestinal Inflammation |
| title_fullStr | Genetic Factors in Animal Models of Intestinal Inflammation |
| title_full_unstemmed | Genetic Factors in Animal Models of Intestinal Inflammation |
| title_short | Genetic Factors in Animal Models of Intestinal Inflammation |
| title_sort | genetic factors in animal models of intestinal inflammation |
| url | http://dx.doi.org/10.1155/1995/604564 |
| work_keys_str_mv | AT rbalfoursartor geneticfactorsinanimalmodelsofintestinalinflammation |