Project description:Improper use of antibiotics in swine could reduce commensal bacteria and possibly increase pathogen infections via the gut resistome. This study aimed to compare the metaproteomic profiles of gut resistome and related metabolism in the cecal microbiota of fattening pigs raised under antibiotic-free (ABF) conditions with those of ordinary industrial pigs (CTRL).
Project description:Bacteroidaceae are common gut microbiota members in all warm-blooded animals. However, if Bacteroidaceae are to be used as probiotics, the species selected for different hosts should reflect the natural distribution. In this study, we therefore evaluated host adaptation of bacterial species belonging to the family Bacteroidaceae. B. dorei, B. uniformis, B. xylanisolvens, B. ovatus, B. clarus, B. thetaiotaomicron and B. vulgatus represented human-adapted species while B. gallinaceum, B. caecigallinarum, B. mediterraneensis, B. caecicola, M. massiliensis, B. plebeius and B. coprocola were commonly detected in chicken but not human gut microbiota. There were 29 genes which were present in all human-adapted Bacteroides but absent from the genomes of all chicken isolates and these included genes required for the pentose cycle, and glutamate or histidine metabolism. These genes were expressed during an in vitro competitive assay, in which human-adapted Bacteroides species overgrew the chicken adapted isolates. Not a single gene specific for the chicken-adapted species was found. Instead, chicken adapted species exhibited signs of frequent horizontal gene transfer, of KUP, linA and sugE genes in particular. The differences in host adaptation should be considered when the new generation of probiotics for humans or chickens is designed.
Project description:Short-chain fatty acids (SCFAs) are the end-products of bacterial fermentation of dietary fibre, and can play a crucial role in regulating immunity and metabolism in the gut and peripheral tissues. Here we show that butyrrate, an SCFA, displayed antiviral effects in chicken respiratory epithelial cells, likely via the regulation of interferon-stimulated genes, particularly OASL. The observed antiviral signaling mechanism would involve HDAC inhibition and Sp1-dependent regulation of the OASL promoter, shedding light on new mechanisms through which the GM regulates poultry mucosal immunity along the gut-lung axis in the chicken.
Project description:The gut of chicken is mostly colonised with Campylobacter jejuni and with 100 fold less C. coli. The competitive ability of C. coli OR12 over C. jejuni OR1 has been examined in experimental broiler chickens following the observation that C. coli replaced an established C. jejuni intestinal colonisation within commercial chicken flocks reared outdoors (El-Shibiny, A., Connerton, P.L., Connerton, I.F., 2005. Enumeration and diversity of campylobacters and bacteriophages isolated during the rearing cycles of free-range and organic chickens. Applied Environmental Microbiology. 71, 1259-1266).
Project description:Campylobacter jejuni is the major cause of acute gastroenteritis in the developed world. It is usually acquired through contaminated poultry as C. jejuni causes a silent asymptomatic infection of the chicken. Pathogens face different sources of stress during its transit through the gut. In this study, we describe the ability of C. jejuni to survive nitrosative stress at very low oxygen levels that reflect those in hypoxic gut environments. Specifically, we here explore an innovative model of signal recognition during colonization. We use a diffusion capsule to feed small, diffusible molecules from chicken caecal matter into a microaerobic C. jejuni culture to study the transcriptomic changes mounted as response to chemical signals present in the chicken gut. We find that in early stages of exposure to the caecal contents (10 min) the dual component colonization regulator, dccR, plays an important yet not fully understood role. Although the caecal material contains cyanide derived from plant sources, we find no role for a truncated globin (encoded by ctb), which has previously been implicated in resistance to this haem ligand.