Germ-free and barrier-raised TGF beta 1-deficient mice have similar inflammatory lesions
Germ-free and barrier-raised TGF beta 1-deficient mice have similar inflammatory lesions
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DOI：
10.1023/a:1018490007745
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发表时间：
1997-05-01
影响因子：
3
通讯作者：
Doetschman, T
中科院分区：
文献类型：
--
作者：
Boivin, GP;JonesCarson, J;Doetschman, T
屏障升高的转化生长因子β 1（TGF β 1）缺陷型小鼠在35日龄前始终死于严重的多器官炎性疾病，该疾病可影响骨骼肌、心脏、肝脏、胰腺、唾液腺、肺、食管和胃。这种疾病的根本原因尚不清楚。为了确定免疫系统对肠道植物群的存在的异常应答是否起致病作用，在无菌环境中饲养TGF β 1缺陷型和野生型小鼠的群体。检查了7只无菌TGF β 1缺陷型小鼠和5只无菌TGF β 1野生型小鼠。对50只屏障升高的TGF β 1突变小鼠和32只屏障升高的野生型小鼠的病变发展进行分析并与历史数据进行比较。所有无菌TGF β 1缺陷小鼠在意义后不久死亡，就像它们的屏障提高的对应物一样。无菌TGF β 1缺陷小鼠的死亡时间明显延迟于屏障升高突变小鼠。然而，在无菌或屏障条件下饲养的TGF β 1突变小鼠之间的病变类型、严重程度或发生率没有差异。无菌野生型小鼠无病变。可以得出结论，微生物在TGF β 1缺陷小鼠的疾病诱导中发挥最小的作用。
Barrier-raised transforming growth factor beta 1 (TGF beta 1)-deficient mice consistently die before 35 days of age of a severe multiorgan inflammatory disease that can affect the skeletal muscle, heart, liver, pancreas, salivary gland, lung, oesophagus and stomach. The underlying cause of this disease is not known. To determine whether abnormal responsiveness of the immune system to the presence of enteric flora plays a causative role, a colony of TGF beta 1-deficient and wild-type mice were raised in a sterile environment. Seven germ-free TGF beta 1-deficient and 5 germfree TGF beta 1 wild-type mice were examined. Lesion development was analysed and compared with historical data on 50 barrier-raised TGF beta 1 mutant mice and 32 barrier-raised wild-type mice. All germ-free TGF beta 1-deficient mice died shortly after meaning, as do their barrier-raised counterparts. There was a significant delay in death in germ-free TGF beta 1-deficient mice compared with barrier-raised mutant mice. However, there was no difference in the type, severity or incidence of lesions between TGF beta 1 mutant mice raised under germ-free or barrier conditions. Germ-free wild-type mice had no lesions. It is concluded that microorganisms play a minimal role in disease induction in TGF beta 1-deficient mice.