Subchronic oral mercury caused intestinal injury and changed gut microbiota in mice.

Mercury is a key global pollutant, yet the mechanism by which mercury-exposure causes intestinal injury is not clear, we aimed to investigate the mechanism of intestinal injury and gut microbiota changes caused by mercury-exposure. Twelve Kunming mice were divided into two groups (n = 6), and the two groups were treated with 0 mg/L and 80 mg/L HgCl2 in drinking water for 90 days respectively. Our results showed that mercury-exposure prominently effected body weight gain and glucose levels. The mercury-exposed mice showed intestinal injury, which was diagnosed by Histopathological Examination and Transmission Electron Microscopy. Meanwhile, RT-PCR indicated that mercury-exposure significantly increased the expression of pro-apoptotic genes including Bax, JNK, ASK1, caspase3 and TNF-α, and significantly decreased the expression of the anti-apoptotic gene Bcl-2. Furthermore, high-throughput sequencing analysis showed that at the genus level some microbial populations including Coprococcus, Oscillospira and Helicobacter were significantly increased whereas some microbial populations including Lgnatzschineria, Salinicoccus and Bacillus were significantly decreased. Moreover, PICRUSt analysis revealed potential metabolic changes. Correlation analysis indicated that microorganisms were significantly correlated with apoptotic gene expression. In summary, our results indicated that mercury-exposure affected the growth and development of mice, induced intestinal microbiota dysbiosis and metabolic disorder, and aggravated apoptosis in mice.

A Multi-Omics Study of Chicken Infected by Nephropathogenic Infectious Bronchitis Virus.

Chicken gout resulting from nephropathogenic infectious bronchitis virus (NIBV) has become a serious kidney disease problem in chicken worldwide with alterations of the metabolic phenotypes in multiple metabolic pathways. To investigate the mechanisms in chicken responding to NIBV infection, we examined the global transcriptomic and metabolomic profiles of the chicken's kidney using RNA-seq and GC-TOF/MS, respectively. Furthermore, we analyzed the alterations in cecal microorganism composition in chickens using 16S rRNA-seq. Integrated analysis of these three phenotypic datasets further managed to create correlations between the altered kidney transcriptomes and metabolome, and between kidney metabolome and gut microbiome. We found that 2868 genes and 160 metabolites were deferentially expressed or accumulated in the kidney during NIBV infection processes. These genes and metabolites were linked to NIBV-infection related processes, including immune response, signal transduction, peroxisome, purine, and amino acid metabolism. In addition, the comprehensive correlations between the kidney metabolome and cecal microbial community showed contributions of gut microbiota in the progression of NIBV-infection. Taken together, our research comprehensively describes the host responses during NIBV infection and provides new clues for further dissection of specific gene functions, metabolite affections, and the role of gut microbiota during chicken gout.