Extended Data Figure 9 : CCM formation is stimulated by spontaneous abscess formation and not blocked by vancomycin.

From: Endothelial TLR4 and the microbiome drive cerebral cavernous malformations

Extended Data Figure 9

a, P10 hindbrains from generation 3/post-ABX Krit1ECKO littermates in the longitudinal antibiotic experiment described in Fig. 6e–l. The animal with a large CCM lesion burden on the far right was found to have an abdominal abscess (circle, ‘absc’) and splenomegaly (arrow, lower right). Scale bar, 1 mm. b, Schematic of the experimental design in which cohoused, lesion susceptible Krit1ECKO mating pairs were used to test the acute effect of vancomycin treatment on CCM formation. Offspring were studied after receiving maternal vehicle or vancomycin administered from E14.5 to P11. c, d, Visual images of hindbrains from representative offspring following vehicle or vancomycin antibiotic treatment. Scale bars, 1 mm. e, f, Volumetric quantification of CCM lesions and brain volumes in Krit1ECKO littermates treated with vehicle or vancomycin. g, h, Relative quantification of total neonatal gut bacterial load measured by qPCR of bacterial universal 16S or Firmicutes-specific rRNA gene copies. n ≥ 6 per group. Error bars of all graphs shown as s.e.m. and significance determined by unpaired, two-tailed Student’s t-test. n.s., P > 0.05. ****P < 0.0001.