Toll样受体2基因敲除小鼠模型

对目标突变纯合的小鼠是有活力的，大小正常，没有任何明显的身体或行为异常。 通过分离的腹膜巨噬细胞的蛋白质印迹分析未检测到基因产物（蛋白质）。 骨髓衍生的巨噬细胞对螺旋体（Borrelia burgdorferi）脂蛋白激发无反应，尽管非脂蛋白超声处理可激活细胞。 通过后踝肿胀评估，由于伯氏疏螺旋体感染引起的关节炎在突变小鼠中更为严重。 被感染突变体的组织所含细菌水平比野生同窝幼虫高100倍。 感染后8周，螺旋体数量增加。 纯合子不产生TNF-α或IL-6，并且在用钩端螺旋体（问号）脂多糖（LPS）治疗时不会出现疾病症状。 该突变小鼠品系可能在研究宿主对细菌内毒素（如败血性休克）的反应中有用。

Homozygous mutant mice targeting the gene of interest are viable, normal in size, and display no overt physical or behavioral abnormalities. No gene product (protein) was detected via western blot analysis of isolated peritoneal macrophages. Bone marrow-derived macrophages failed to respond to stimulation with Borrelia burgdorferi lipoproteins, though non-lipoprotein sonicates were able to activate these cells. Arthritis induced by Borrelia burgdorferi infection was more severe in the mutant mice, as assessed by hind ankle swelling. Tissues from infected mutant mice harbored 100-fold higher bacterial loads than those of wild-type littermate mice. The spirochete burden increased by 8 weeks post-infection. Homozygous mutants did not produce TNF-α or IL-6, and showed no disease symptoms when treated with Leptospira (?) lipopolysaccharide (LPS). This mutant mouse line may be useful for studying host responses to bacterial endotoxins such as septic shock.

搜集汇总

背景与挑战

背景概述

该数据集提供了Toll样受体2基因敲除小鼠模型的详细信息，包括其表型特征、对细菌感染的免疫反应变化，以及该模型在研究宿主对细菌内毒素（如败血性休克）反应中的潜在应用。数据集还包含了资源的共享方式、申请流程及联系信息。