Article Figures & Data
Figures
- FIG 1
Alteration of fecal bile acid metabolism in infantile cholestasis. The levels of primary and secondary bile acids in the cohort of infants with cholestatic jaundice (CJ) or impaired hepatic function (IHF) and the health controls (HC) were measured by tandem mass spectrometry. Significant differences were determined by one-way analysis of variance (ANOVA) followed by Tukey’s post hoc test. ns, not significant; *, P < 0.05; **, P < 0.01; ***, P < 0.001. HCA, hyocholic acid; 3_DHCA, 3-dehydrocholic acid; 7_DHCA, 7-dehydrocholic acid; KLCA, ketolithocholic acid; UCA, ursocholic acid; bUCA, β-ursocholic acid; muroCA, murocholic acid; NorCA, norcholic acid.
- FIG 2
Comparison of the taxonomic diversity of the gut microbiomes among the cholestatic jaundice (CJ), impaired hepatic function (IHF), and healthy control (HC) groups. The gut microbiota alpha diversity was measured from the Shannon (A) and Chao1 (B) indexes. The Wilcoxon test was performed for pairwise comparisons. *, P < 0.05; **, P < 0.01; ***, P < 0.001. (C) PCoA of Bray-Curtis distances generated from taxa summarized at the genus level. Each point corresponds to a sample shaped and colored by diagnosis.
- FIG 3
Significant differences between the gut bacterial taxa of the cholestatic jaundice (CJ), impaired hepatic function (IHF), and healthy control (HC) groups. Comparisons among the groups were performed using one-way analysis of variance (ANOVA; P < 0.05). The Wilcoxon test was performed for pairwise comparisons, *, P < 0.05; **, P < 0.01; ***, P < 0.001. g, genus; s, species; f, family.
- FIG 4
Discrepancy in microbial community phenotypes between the cholestatic jaundice (CJ) group and the other two groups. BugBase identified phenotypes associated with aerobic bacteria (A), anaerobic bacteria (B), facultatively anaerobic bacteria (C), oxidative stress tolerance (D), Gram-negative bacteria (E), Gram-positive bacteria (F), mobile element content (G), biofilm formation (H), and pathogenesis (I). Statistical significance was identified by the Wilcoxon test with false discovery rate (FDR)-corrected pairwise P values. *, P < 0.05; **, P < 0.01; ***, P < 0.001.
- FIG 5
Functional alterations of the gut microbiome in infants with cholestatic jaundice (CJ) and impaired hepatic function (IHF). Statistical significance was determined by using LEfSe, with a P value of <0.05 (Wilcoxon test) and a linear discriminant analysis (LDA) score (log10) of >3 being considered significant.
- FIG 6
Correlation matrices constructed from gut bacterial taxa, fecal BAs, and serum indicators of hepatic function. Spearman correlation analysis between fecal BA serum indicators of hepatic function and the top 17 OTUs with significantly different abundances among the groups (A) and the gut microbiota functional categories (B) was employed. Four distinct OTU clusters (clusters O1 to O4) and two distinct functional clusters (clusters F1 and F2) were observed. Red and blue represent the positive and negative correlations, respectively. GHDCA, glycohyodeoxycholic acid; TCA, taurocholic acid; GCA, glycocholic acid; LCA, lithocholic acid; GLCA, glycolithocholic acid; THDCA, taurohyodeoxycholic acid; TLCA-3S, taurolithocholic acid-3-sulfate acid; GCDCA, glycochenodeoxycholic acid; GHCA, glycohyocholic acid; TUDCA, tauroursodeoxycholic acid; GDCA, glycodeoxycholic acid; THCA, taurohyocholic acid; TDCA, taurodeoxycholic acid; GUDCA, glycoursodeoxycholic acid; ALB, albumin; ALT, alanine aminotransferase; AST, aspartate aminotransferase; BA, bile acid; DB, direct bilirubin; HB, hemoglobin; GGT, gamma-glutamyltransferase; TB, total bilirubin.
Tables
- TABLE 1
Characteristics of infants with CJ, IHF, and HCa
↵a ALB, albumin; ALT, alanine aminotransferase; AST, aspartate aminotransferase; BA, bile acid; DB, direct bilirubin; HB, hemoglobin; GGT, gamma-glutamyltransferase; TB, total bilirubin; IQR, interquartile range; CMV, cytomegalovirus; HC, health control; IHF, impaired hepatic function; CJ, cholestatic jaundice.
↵b Two infants had Alagille syndrome with a Jagged 1 (JAG1) mutation, four had citrin deficiency with a solute carrier family 25 member 13 (SLC25A13) mutation, and two had BA synthesis defects with aldo-keto reductase family 1 member D1 (AKR1D1) mutation.
↵c The data were compared by the nonparametric Mann-Whitney test (two groups) or Kruskal-Wallis H test (multiple groups). The distribution of dichotomous variables was compared by the chi-squared test.
TABLE S1
OTUs with significantly different abundances among the cholestatic jaundice (CJ), impaired hepatic function (IHF), and healthy control (HC) groups. Download Table S1, DOCX file, 1.0 MB.
Copyright © 2019 Wang et al.
This content is distributed under the terms of the Creative Commons Attribution 4.0 International license.
FIG S1
Rarefaction analysis of the 16S rRNA genes in the fecal microbiome. Rarefaction plots of all 126 samples show the number of observed OTUs reaching the asymptote at the cutoff of 10,000 reads. Each sample is represented by a different color in the graph. Download FIG S1, TIF file, 1.0 MB.
Copyright © 2019 Wang et al.
This content is distributed under the terms of the Creative Commons Attribution 4.0 International license.
