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Influence of Deoxynivalenol-contaminated diet on the liver gene expression of chicken.

ABSTRACT: The mycotoxin deoxynivalenol (DON) is a secondary metabolite from Fusarium species and is frequently present on wheat and other cereals. The main effects of DON are a reduction of the feed intake and reduced weight gain of broilers. At the molecular level DON binds to the 60S ribosomal subunit and inhibits subsequently protein synthesis at the translational level. It has been suggested that cells and tissues with high protein turnover rate, like the liver and small intestine, are most affected by DON. However, little is known about other effects of DON e.g. at the transcriptional level. Therefore we decided to perform a microarray analysis, which allows us the investigation of thousands of transcripts in one experiment.

ORGANISM(S): Gallus gallus

PROVIDER: GSE25185 | GEO | 2011/11/05

SECONDARY ACCESSION(S): PRJNA134531

REPOSITORIES: GEO

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Project description:Deoxynivalenol (DON) is a type B trichothecene mycotoxin that is commonly found in cereals and grains worldwide. The presence of this fungal secondary-metabolite raises public-health concerns at both the agriculture and food industry level. The toxicity of DON is mainly characterized by its ability to inhibit ribosomal protein biosynthesis. Recently, we have shown that DON has a negative impact on gut integrity, a feature also noticed for Campylobacter (C.) jejuni. We further demonstrated that DON increased the load of C. jejuni in the gut and inner organs. In contrast, feeding the less toxic DON metabolite deepoxy-deoxynivalenol (DOM-1) to broilers reduced the Campylobacter load in vivo. Consequently, it can be hypothesized that DON and DOM-1 have a direct or indirect effect on the growth profile of C. jejuni. The aim of the present study was to further resolve the nature of this interaction in vitro by co-incubation and RNA-sequencing. The co-incubation of C. jejuni with DON resulted in significantly higher bacterial growth rates from 30 h of incubation onwards. On the contrary, the co-incubation of C. jejuni with DOM-1 reduced the CFU counts, indicating that this DON metabolite might contribute to reduce the burden of C. jejuni in birds, altogether confirming in vivo data. Furthermore, the transcriptomic profile of C. jejuni following incubation with either DON or DOM-1 differed. Co-incubation of C. jejuni with DON significantly increased the expression of multiple genes which are critical for Campylobacter growth, particularly members of the Flagella gene family, frr (ribosome-recycling factor), PBP2 futA-like (Fe3+ periplasmic binding family) and PotA (ATP-binding subunit). These organelles are required for pathogenicity-related phenotypes including motility, biofilm formation, host cell interactions, and host colonization, which may explain the high Campylobacter load in the intestine of DON-fed broiler chickens. On the contrary, DOM-1 downregulated the Flagella gene family and upregulated ribosomal proteins. The results highlight the adaptive mechanisms involved in the transcriptional response of C. jejuni to DON and its metabolite DOM-1, based on the following effects: (a) ribosomal proteins; (b) flagellar proteins; (c) engagement of different metabolic pathways. The results provide insight into the response of an important intestinal microbial pathogen against DON and lead to a better understanding of the luminal or environmental acclimation mechanisms in chickens.

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Influence of Deoxynivalenol-contaminated diet on the liver gene expression of chicken.

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