When Mark Kahn and his team needed to transfer their mice to a new facility, they were worried that the move might disrupt their experiments. The group had been working with models of cerebral cavernous malformations—collections of enlarged and abnormally shaped capillaries that are vulnerable to haemorrhage, giving rise to seizures and stroke. In the old facility, mice with specific mutations had reliably developed lesions similar to the pathology seen in humans. So, when this phenotype suddenly disappeared following the move to the new facility, the group initially thought their fears had been realized. ‘But then came a piece of serendipity’, says Kahn, who is based at the University of Pennsylvania. ‘A small number of the mice developed a peritoneal abscess … And those animals were the only ones to exhibit significant lesions’. Suspecting that the infection had helped re-establish the phenotype, the group showed that injecting the mutant mice with gram-negative bacteria, or lipopolysaccharide—a component of the gram-negative cell wall—restored lesion formation. Cross-fostering mutant pups to animals that had been reared in another facility also had the same effect. The results thus suggested that bacteria were contributing to the expression of a genetic brain disease (Tang et al., 2017).

中文翻译：

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“所有疾病都始于肠道”：希波克拉底对吗？

当马克·卡恩（Mark Kahn）和他的团队需要将小鼠转移到新设施时，他们担心这一举动可能会破坏他们的实验。该小组一直在研究脑海绵状畸形的模型，这些模型是易受出血影响，引起癫痫发作和中风的大量毛细血管和异常形状的毛细血管的集合。在旧设施中，具有特定突变的小鼠已经可靠地发展出类似于人类所见病理的病变。因此，当这种表型在转移到新设施后突然消失时，该小组最初认为他们的恐惧已经实现。宾夕法尼亚大学的卡恩说：“但是后来出了意外。” “少数小鼠出现了腹膜脓肿……而这些动物是唯一表现出明显病变的动物”。该小组怀疑感染已帮助重新建立了表型，结果表明，向突变小鼠注射革兰氏阴性细菌或脂多糖（革兰氏阴性细胞壁的组成部分）可以恢复病变的形成。对在另一家机构饲养的动物进行交叉培育的突变幼仔也具有相同的效果。因此结果表明细菌有助于遗传性脑疾病的表达（唐等。，2017）。