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Endothelial TLR4 and the microbiome drive cerebral cavernous malformations

 Nature. 2018; 
Alan T. Tang , Jaesung P. Choi , Jonathan J. Kotzin,, Yiqing Yang , Courtney C. Hong , Nicholas Hobson, Romuald Girard, Hussein A. Zeineddine, Rhonda Lightle, Thomas Moore, Ying Cao, Robert Shenkar, Mei Chen , Patricia Mericko , Jisheng Yang , Li Li , Ceylan Tanes, Dmytro Kobuley, , Urmo Võsa, Kevin J. Whitehead, Dean Y. Li, Lude Franke, Blaine Hart0, Markus Schwaninger, Jorge Henao-Mejia,,, Leslie Morrison0, Helen Kim, Issam A. Awad, Xiangjian Zheng,, & Mark L. Kahn
Products/Services Used Details Operation
Mouse IL-1β was purchased from Genscript (Z02988) and administered to the resistant Ccm2ECKO neonatal CCM disease model. At P5, a 5ng dose of IL-1β dissolved in sterile PBS was administered retro-orbitally in a total 30μl volume by 31-gauge needle. At P10, an 8-ng dose of IL-1β was administered retro-orbitally in a total 50μl volume by 31-gauge needle

摘要

Cerebral cavernous malformations (CCMs) are a cause of stroke and seizure for which no effective medical therapies yet exist. CCMs arise from the loss of an adaptor complex that negatively regulates MEKK3–KLF2/4 signalling in brain endothelial cells, but upstream activators of this disease pathway have yet to be identified. Here we identify endothelial Toll-like receptor 4 (TLR4) and the gut microbiome as critical stimulants of CCM formation. Activation of TLR4 by Gram-negative bacteria or lipopolysaccharide accelerates CCM formation, and genetic or pharmacologic blockade of TLR4 signalling prevents CCM formation in mice. Polymorphisms that increase expression of the TLR4 gene or the gene encoding its co-rece... More

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