正文
为测试抗生素能否影响基因变异小鼠的损伤发展情况，科研人员喂养了几代小鼠，给它们的亲代小鼠注入抗生素，测试之后每一代的损伤情况及肠道的菌群数量。
正如他们在无菌条件下喂养的小鼠中发现的那样，细菌下降率为96%，与损伤下降率相近。
以抗生素破坏免疫系统可能不是一种直接的解决方法，当然，我们也不得不牢记老鼠和人类间的潜在不同。我们仍在了解人类的菌群多么复杂，以及多数的健康条件与消化系统微生物多样性相关。然而，针对目前有限的治疗方式，阻止易感损伤方法的新发现无疑是一个重大的突破。
该研究已发表在《自然》杂志。
原文链接：
http://www.sciencealert.com/researchers-find-gut-bacteria-can-trigger-brain-lesions-that-lead-to-strokes
论文基本信息
【题目】Endothelial TLR4 and themicrobiome drive cerebral cavernous malformations
【作者】Alan T. Tang, Jaesung P.Choi, Jonathan J. Kotzin, et al.
【期刊】Nature
【日期】18 May 2017
【DOI】10.1038/nature22075
【地址】
http://www.nature.com/nature/journal/v545/n7654/full/nature22075.html
【摘要】
Cerebral cavernous malformations (CCMs) are a cause ofstroke and seizure for which no effective medical therapies yet exist. CCMsarise from the loss of an adaptor complex that negatively regulates MEKK3–KLF2/4 signalling in brain endothelial cells, but upstreamactivators of this disease pathway have yet to be identified. Here we identifyendothelial Toll-like receptor 4 (TLR4) and the gut microbiome as criticalstimulants of CCM formation. Activation of TLR4 by Gram-negative bacteria orlipopolysaccharide accelerates CCM formation, and genetic or pharmacologicblockade of TLR4 signalling prevents CCM formation in mice. Polymorphisms thatincrease expression of the TLR4 gene or the gene encoding itsco-receptor CD14 are associated with higher CCM lesion burden in humans.Germ-free mice are protected from CCM formation, and a single course ofantibiotics permanently alters CCM susceptibility in mice. These studiesidentify unexpected roles for the microbiome and innate immune signalling inthe pathogenesis of a cerebrovascular disease, as well as strategies for itstreatment.
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