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首页> 外文期刊>Genomics >Genetic analysis of susceptibility to dextran sulfate sodium-induced colitis in mice.
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Genetic analysis of susceptibility to dextran sulfate sodium-induced colitis in mice.

机译：小鼠对葡聚糖硫酸钠引起的结肠炎敏感性的遗传分析。

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摘要

The genetic basis for differential sensitivity of inbred mice to inflammatory bowel disease induced by dextran sulfate sodium (DSS) is unknown. Susceptible C3H/HeJ were outcrossed to partially resistant C57BL/6J mice. F2 and N2 progeny were phenotyped by evaluating histopathologic lesions in large intestine detected 16 days after a 5-day period of feeding 3.5% DSS. Screening for DSS colitis (Dssc) loci revealed quantitative trait loci (QTL) on Chr 5 (Dssc1) and Chr 2 (Dssc2). These traits contributed additively, explaining 17.5% of the variation in total colonic lesions. Additional QTL on Chr 18 and 1 that collectively explained 11% of the variation in total colon lesions were indicated. In the cecum, only a putative QTL on Chr 11 was associated with pathology (lesion severity) in the cecum. Reduced DSS susceptibility was observed in congenic stocks in which the highly susceptible NOD/Lt strain carried putative resistance alleles from either B6 on Chr 2 or from the highly resistant NON/Lt strain on Chr 9. We conclude that multiple genes control susceptibility to DSS colitis in mice. Possible Dssc candidate genes are discussed in terms of current knowledge of inflammatory bowel disease susceptibility loci in humans. Copyright 1999 Academic Press.
机译：近交小鼠对葡聚糖硫酸钠（DSS）引起的炎症性肠病的敏感性差异的遗传基础尚不清楚。易感的C3H / HeJ与部分耐药的C57BL / 6J小鼠杂交。在喂食3.5％DSS的5天后16天，通过评估在大肠中检测到的组织病理学损伤来对F2和N2后代进行表型分析。 DSS结肠炎（Dssc）基因座的筛选揭示了Chr 5（Dssc1）和Chr 2（Dssc2）上的数量性状基因座（QTL）。这些特征相加，解释了总结肠病变的17.5％的变化。还显示了Chr 18和Chr 1上的其他QTL，这些QTL共同解释了总结肠损伤变化的11％。在盲肠中，仅在Chr 11上的假定QTL与盲肠的病理学（病变严重程度）有关。在高敏感的NOD / Lt菌株携带来自Chr 2上的B6或来自Chr 9的高抗性NON / Lt菌株的假定抗性等位基因的同基因种群中，DSS敏感性降低。我们得出结论，多个基因控制着对DSS结肠炎的敏感性在小鼠中。根据人类炎症性肠病易感基因座的最新知识讨论了可能的Dssc候选基因。版权所有1999 Academic Press。

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