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. 2020 Feb 5;8(2):211.
doi: 10.3390/microorganisms8020211.

The Dysbiosis of Gut Microbiota Caused by Low-Dose Cadmium Aggravate the Injury of Mice Liver through Increasing Intestinal Permeability

Yehao Liu  1 , Yuhui Li  2 , Yuhong Xia  1 , Kaiyong Liu  1 , Lingling Ren  1 , Yanli Ji  1
Affiliations

The Dysbiosis of Gut Microbiota Caused by Low-Dose Cadmium Aggravate the Injury of Mice Liver through Increasing Intestinal Permeability

Yehao Liu et al. Microorganisms. .

Abstract

Cadmium (Cd), widely present in food and drinking water at low doses, can cause health risks. However, the mechanistic effects of long-term Cd exposure at low dose through dietary intake is poorly studied. The aim of this study is to elucidate whether the dysbiosis of gut microbiota caused by Cd at an environmental low dose can aggravate the injury of mice liver, and the possible mechanism is investigated. In order to explore the potential underlying mechanism, the analyses of the variation of gut microbiota composition, intestinal permeability, and hepatic transcriptome were conducted. Our results showed that gut microbiota was disturbed. The rise of intestinal permeability induced by the dysbiosis of gut microbiota resulted in more Cd ions accumulating in mice liver, but it could be restored partly through depleting gut microbiota by antibiotics cocktail. Transcriptomic analyses indicated that 162 genes were significantly differentially expressed including 59 up-regulated and 103 down-regulated in Cd treatment. These genes were involved in several important pathways. Our findings provide a better understanding about the health risks of cadmium in the environment.

Keywords: cadmium; gut microbiota; intestinal permeability; transcriptome analyses.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Alpha diversity and intragroup beta diversity of the control and low Cd treatment groups; * p < 0.05.
Figure 2
Figure 2
The plot generated by the weighted UniFrac-based PCoA.
Figure 3
Figure 3
The relative abundance of predominant bacteria at the phylum level in the control and low Cd treatment groups.
Figure 4
Figure 4
The most differentially abundant taxa between the control and low Cd treatment groups which was identified through the LDA score generated from linear discriminant analysis effect size (LEfSe) analysis.
Figure 5
Figure 5
Fluorescein-isothiocyanate-dextran (FITC-dextran) levels in serum from the control and low Cd treatment groups as a measure of intestinal permeability. * p < 0.05.
Figure 6
Figure 6
Levels of mRNA expression of the tight junction proteins from the control and low Cd treatment groups. Results are expressed as mean values (fold change respect to control). * p < 0.05.
Figure 7
Figure 7
The relative abundance of A. mucinipbila in the control and low Cd treatment groups. * p < 0.05.
Figure 8
Figure 8
Cd concentration in mice livers. ** p < 0.01, *** p < 0.001.
Figure 9
Figure 9
The activities of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in serum samples from the control and low Cd treatment groups. ** p < 0.01.
Figure 10
Figure 10
Venn diagram represents the numbers of overlapping genes between control and Low Cd treatment.
Figure 11
Figure 11
Kyoto Encyclopedia of Genes and Genomes (KEGG) database enrichment classification of differentially expressed genes (DEGs).
See this image and copyright information in PMC

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