Extended Data Fig. 2: Changes in microbiota composition are not likely to be associated with the development in VHS.
From: Local immune response to food antigens drives meal-induced abdominal pain
a, changes in the gut microbiome composition over time studied by ordination (PCA) plot before the infection, 10 days after infection (R2 = 0.11, p-value = 0.02), and after OVA gavage (R2 = 0.18, p-value = 0.002) between OVA/infected and saline/infected (n = 8/group) mice. The numbers in brackets indicate the variation explained by each axis (PCA: principal component analysis). b–d, drivers of variation in the murine intestinal community after OVA re-exposure. b, Comparison of mean abundance of taxa between OVA- and saline-infected mice. Bacterial abundances were computed using centred log-ratio transformation (CLR; two-sided Mann–Whitney test, FDR <0.2). c, ordination biplot of PCA analysis showing the significant contributors in the community variation. Arrows indicate the relative importance of each genus (permutation-based P < 0.05). d, abundance of genus Robinsoniella, Eisenbergiella, Senegalimassilia, Murimonas, Clostridium_XVIII and Stomatobaculum by group and VHS (two-sided Mann–Whitney test, FDR >0.1). e, scheme illustrating the post-infectious protocol in mice treated with antibiotics. f, g, VMR to colorectal distention in VHS (OVA/infected + OVA) mice treated with antibiotics or control, and compared to OVA/infected + saline mice (n = 10, 7 and 6, respectively) (g depicts the VMM response at 7 weeks post-infection). In d, VHS threshold was established based on the 95th percentile of visceromotor responses at baseline (AUC >4.8). There was no significant association between VHS and bacterial abundance in any group (two-tailed Mann–Whitney test). X-axis indicates absence (0) and presence (1) of VHS. Two-way ANOVA 9(Sidak’s multiple-comparisons test) in f and g. Data shown as box-and-whiskers ± 1.5 IQR in d and as median ± IQR in f and g. VMR, visceromotor response; BL, baseline; w, week.
