Feces metagenome
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1056821 | ENA |
REPOSITORIES: ENA
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Project description:The foodborne illness is the important public health concerns, and the livestock feces are known to be one of the major reservoirs of foodborne pathogens. Also, it was reported that 45.5% of foodborne illness outbreaks have been associated with the animal products contaminated with the livestock feces. In addition, it has been known that the persistence of a pathogens depends on many potential virulent factors including the various virulent genes. Therefore, the first step to understanding the public health risk of livestock feces is to identify and describe microbial communities and potential virulent genes that contribute to bacterial pathogenicity. We used the whole metagenome shotgun sequencing to evaluate the prevalence of foodborne pathogens and to characterize the virulence associated genes in pig and chicken feces. Our data showed that the relative abundance of potential foodborne pathogens, such as Bacillus cereus was higher in chickens than pigs at the species level while the relative abundance of foodborne pathogens including Campylobacter coli was only detected in pigs. Also, the microbial functional characteristics of livestock feces revealed that the gene families related to "Biofilm formation and quorum sensing" were highly enriched in pigs than chicken. Moreover, the variety of gene families associated with "Resistance to antibiotics and toxic compounds" were detected in both animals. These results will help us to prepare the scientific action plans to improve awareness and understanding of the public health risks of livestock feces.
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Project description:BACKGROUND & AIMS: Recent studies revealed that hemoglobin is expressed in some non-erythrocytes and it suppresses oxidative stress when overexpressed. Oxidative stress plays a critical role in the pathogenesis of non-alcoholic steatohepatitis (NASH). This study was to investigate whether hemoglobin is expressed in hepatocytes and how it is related to oxidative stress in NASH patients. METHODS: Microarray was performed to identify differentially expressed genes in NASH. Quantitative real time PCR (qRT-PCR) was used to examine gene expression levels. Western blotting and immunofluorescence staining were employed to examine hemoglobin proteins. Flow cytometry was used to measure intracellular oxidative stress. RESULTS: Analysis of microarray gene expression data has revealed a significant increase in the expression of hemoglobin alpha (HBA1) and beta (HBB) in liver biopspies from NASH patients. Increased hemoglobin expression in NASH was validated by qRT-PCR. However, the expression of erythrocyte specific marker genes such as SPTA, SPTB, GYPA, GATA1, and ALAS2 did not change, indicating that increased hemoglobin expression in NASH was not from erythropoiesis, but could result from increased expression in hepatocytes. Immunofluorescence staining demonstrated positive HBA1 and HBB expression in the hepatocytes of NASH livers. Hemoglobin expression was also observed in human hepatocellular carcinoma HepG2 cell line. Furthermore, treatment with hydrogen peroxide, a known oxidative stress inducer, induced a dose dependent increase in HBA1 expression in HepG2 cells. Intriguingly, forced hemoglobin expression suppressed oxidative stress. CONCLUSIONS: Oxidative stress upregulates hemoglobin expression in hepatocytes. Suppression of oxidative stress by hemoglobin could be a mechanism to protect hepatocytes from oxidative damage. These findings suggest that hemoglobin is an inducible antioxidant in hepatocytes in response to increased oxidative stress as found in NASH livers. Twelve biopsy diagnosed NASH patients were included in this study. For control groups, total RNA from 5 different subjects were purchased from ADMET. These subjects are free from liver disease.
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Project description:Increased liver de novo lipogenesis (DNL) is a hallmark of nonalcoholic steatohepatitis (NASH). A key enzyme controlling DNL upregulated in NASH is ATP citrate lyase (ACLY). In mice, inhibition of ACLY reduces liver steatosis, ballooning and fibrosis and inhibits activation of hepatic stellate cells. Glucagon like peptide-1 receptor (GLP-1R) agonists lower body mass, insulin resistance and steatosis without improving fibrosis. Here, we find that combining an inhibitor of liver ACLY, bempedoic acid, and the GLP-1R agonist liraglutide reduces liver steatosis, hepatocellular ballooning, and hepatic fibrosis in a mouse model of NASH. Liver RNA analyses revealed additive downregulation of pathways that are predictive of NASH resolution, reductions in the expression of prognostically significant genes compared to clinical NASH samples, and a predicted gene signature profile that supports fibrosis resolution. These findings support further investigation of this combinatorial therapy to treat obesity, insulin resistance, hypercholesterolemia, steatohepatitis, and fibrosis in people with NASH.
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