Fig. 1

The fungal gut microbiota is altered in infants that later develop bronchopulmonary dysplasia. Intestinal microbiome analysis from the first true stool from 102 very low birthweight premature infants (birthweight < 1500 g). A Fungal alpha diversity of infants with moderate to severe bronchopulmonary dysplasia or death prior to 36 weeks of gestation (BPD) to those without (NoBPD) as quantified by the Shannon (p = 0.0010, Mann–Whitney) and Simpson indices (p = 0.0021, Mann–Whitney). Values represent means ± SEM. B Bacterial alpha diversity. C Fungal beta diversity. Principal coordinates analysis (PCoA) of Bray–Curtis dissimilarity displaying differences in fungal beta diversity (p = 0.040, permutational multivariate analysis of ANOVA, PERMANOVA. p = 0.44, permutational multivariate analysis of dispersion, PERMDISP). Ellipses indicate the 95% confidence interval. D Biplot of principal components analysis (PCA) with fungal community composition driven by amplicon sequence variants (ASVs) aligning to the genera Candida and Aureobasidium. PCA is shown in the inset. E Bacterial beta diversity. PCoA of Bray–Curtis dissimilarity displaying bacterial beta diversity (p = 0.06109, PERMANOVA. p = 0.37, PERMDISP). F Biplot of PCA of bacterial community composition. PCA is shown in the inset. G and H SPIEC-EASI network analysis shows that BPD infants formed sparser multikingdom interaction networks than NoBPD infants (fewer fungal than bacterial edges but a similar number of nodes, and lower edge density). See also Fig. S2–3