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. Author manuscript; available in PMC: 2018 Jan 8.
Published in final edited form as: Nature. 2017 May 10;545(7654):305–310. doi: 10.1038/nature22075

Figure 1. CCM formation is stimulated by gram negative bacterial infection and intravenous LPS injection.

Figure 1

a, Lesion formation in susceptible and resistant iECre;Ccm2fl/fl mice at P17. Dotted lines trace cerebellar white matter. Asterisks; CCM lesions Scale bars, 1 mm (left) and 100 μm (right). b, Hindbrains of resistant iECre;Ccm2fl/fl littermates without (top) and with (bottom) spontaneous abdominal gram negative abscess. Scale bars, 1 mm. Arrows; CCM lesions. c, The bacterial abscess (“absc”) identified in (b) contains gram negative bacteria (arrows). Scale bars, 4 mm (top) and 10μm (bottom). d, CCM formation in resistant iECre;Ccm2fl/fl littermates following injection with a live B. fragilis/autoclaved cecal contents mixture (B. fragilis) or ACC alone (ACC vehicle). Scale bars, 1 mm. e–f, Resistant iECre;Ccm2fl/fl responders exhibit splenic abscesses and increased spleen weight compared with non-responders. g, CCM formation in resistant iECre;Ccm2fl/fl mice following vehicle or LPS treatment. Scale bars, 1 mm. h–i, Quantitation of lesion and total brain volumes. Error bars shown as s.e.m. and significance determined by one way ANOVA with Holm-Sidak correction for multiple comparisons or unpaired, two-tailed t-test. **** indicates p<0.0001; ***indicates p<0.001; n.s. indicates p>0.05.