Gastroenterology · 1994
Spontaneous, heritable colitis in a new substrain of C3H/HeJ mice.
СтатьяПоддержка исследования: вне правительства СШАПоддержка службы здравоохранения СШАНазвание и аннотация: Перевод пока не подготовлен
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Sundberg J P, Elson C O, Bedigian H, Birkenmeier E H
Аннотация
BACKGROUND/AIMS: C3H/HeJ mice at the Jackson Laboratory have periodically been culled because of the occurrence of soft feces, perianal ulceration, and right-sided colitis. No pathogens have been isolated. The goal of the current study was to establish a substrain with a high incidence of this disease.
METHODS: Affected male and female C3H/HeJ mice were bred. The clinical, pathological, microbiological, and genetic features of 216 mice of the resulting pedigree were characterized.
RESULTS: A severely affected female crossed with a normal male resulted in a new substrain, denoted C3H/HeJBir, with a high incidence of right-sided colitis. Histologically, lesions occurred primarily in the cecum and proximal colon, characterized by acute and chronic inflammation, crypt abscesses, ulcerations, regenerative hyperplasia, and submucosal scarring. Such colitis peaked at 3-6 weeks; however, similar disease was found sporadically in animals more than 1 year of age. Small lesions at the anorectal junction were common throughout life. An extensive search for pathogens was negative. Genetic analysis of C3H/HeJBir mice suggested that the disease was inherited as a quantitative trait.
CONCLUSIONS: C3H/HeJBir mice develop a spontaneous, heritable form of idiopathic inflammatory bowel disease and will be a valuable resource for genetic and immunologic studies of this disease.
METHODS: Affected male and female C3H/HeJ mice were bred. The clinical, pathological, microbiological, and genetic features of 216 mice of the resulting pedigree were characterized.
RESULTS: A severely affected female crossed with a normal male resulted in a new substrain, denoted C3H/HeJBir, with a high incidence of right-sided colitis. Histologically, lesions occurred primarily in the cecum and proximal colon, characterized by acute and chronic inflammation, crypt abscesses, ulcerations, regenerative hyperplasia, and submucosal scarring. Such colitis peaked at 3-6 weeks; however, similar disease was found sporadically in animals more than 1 year of age. Small lesions at the anorectal junction were common throughout life. An extensive search for pathogens was negative. Genetic analysis of C3H/HeJBir mice suggested that the disease was inherited as a quantitative trait.
CONCLUSIONS: C3H/HeJBir mice develop a spontaneous, heritable form of idiopathic inflammatory bowel disease and will be a valuable resource for genetic and immunologic studies of this disease.