Extended Data Fig. 5: Transcriptional induction of Casp11 in bECs and gene signatures of LPS-challenged mouse brains.

a–c, RNAscope in situ hybridization analyses of Casp11 mRNA in bECs in PBS and LPS-treated mice. a, Representative staining images of Cd31 and Casp11 mRNA in the mouse cortices. DAPI, the nuclei; white arrowheads, Cd31 mRNA⁺ endothelial nuclei co-labelled with Casp11 mRNA signals. b, Quantification of Casp11 mRNA signals in cortical Cd31 mRNA⁺ endothelial nuclei. n = 6,222 and 5,214 Cd31 mRNA⁺ nuclei from 3 PBS- and 3 LPS-treated mice, respectively. c, Percentages of Casp11 mRNA⁺ nuclei among Cd31 mRNA⁺ endothelial nuclei (mean ± s.e.m., n = 3 mice per group). Two-sided Wilcoxon rank-sum test (b) and unpaired two-sided Welch’s t test (c) were used (*p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001; ns, not significant). d, Analyses of the scRNA-seq data (Extended Data Fig. 4) to obtain transcriptional signatures in LPS-challenged WT and Gsdmd^−/− mouse brains. Left, heatmaps of gene expression profile in selected cell types (other cell types had little responses, thus not included). Right, bar plots of signature genes in each row of the heatmap, corresponding to a GO term (1^st row, upregulated in WT but not Gsdmd^−/− cells; 2^nd row, upregulated in Gsdmd^−/− but not WT cells; 3^rd row, downregulated in both WT and Gsdmd^−/− cells; 4^th row, upregulated in both WT and Gsdmd^−/− cells). One-sided Fisher’s exact test with the Benjamini-Hochberg multiple comparisons. See Supplementary Table 1 for detailed statistics. Data (a–c) are representative of three independent experiments.

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