Abstract
Recent metagenomic studies suggest that innate and adaptive immune phenotypes can be programmed via gut microbiota-host interactions mediated via activation of pattern recognition receptors (PRRs) on host cells. In this study, we used two extremely different pig lines (the Yorkshire and the Tibetan) to test the hypothesis that the transplantation of gut microbiota could transfer certain immunologic characteristics from donor to recipient. The faecal microbiota of these two pig lines was transplanted in healthy commercial hybrid newborn piglets to establish the “Tibetan-intervened” and “Yorkshire-intervened” porcine models. Then, acute colitis was induced using dextran sulphate sodium (DSS), which activated Toll-/NOD-like receptor (TLR/NLR) signalling in the colonic tissues of the “Yorkshire-intervened” piglets, leading to increases in pro-inflammatory cytokines and immune cells and causing intestinal injuries. Conversely, DSS administration had little influence on the “Tibetan-intervened” piglets, which showed no significant inflammation and no changes in cytokines, immune cells, or signalling molecules, including TLRs, NLRs, MYD88 and NF-κB, after DSS treatment. These results indicate that pigs inoculated with the Tibetan microbiota acquired relatively strong resistance to experimental colitis, suggesting that the genotype of the host contributes to the uniqueness of its intestinal microbial community, whereas the microbiota plays a vital role in programming the immune phenotypes of the host.
Highlights
The host immune system and the bacterial populations; and disruption of this balance may cause dysbiosis and even an inflammatory response in the host[3]
By tracking (Part II) the phenotypic expression, the pattern recognition receptors (PRRs) signalling pathways and the immune cells in the normal condition and acute colitis models, we show how immune traits can be regulated by altering the gut microbiota through faecal microbiota transplantation (FMT) and how these donor and recipient animals can be used to conduct controlled proof-of-principle “clinical” metagenomic studies of host-microbiome interrelations
We performed a 16S rRNA gene-based survey of faecal specimens obtained from Yorkshire and Tibetan pigs, which consumed the same diet at all times
Summary
The host immune system and the bacterial populations; and disruption of this balance may cause dysbiosis and even an inflammatory response in the host[3]. Another study colonized germ-free (GF) mice with a mouse microbiota or human microbiota and showed that the nature of the colonizing microbiota affected the host’s initial T cell populations[19], providing further evidence for host-linked co-evolution of the microbiota and immune responses These findings are paving the way for the use of the microbiome to improve human health in the near future; our understanding of microbial communities and their interactions with the host is still very limited. By tracking (Part II) the phenotypic expression, the PRR signalling pathways and the immune cells in the normal condition and acute colitis models (induced by dextran sulphate sodium), we show how immune traits can be regulated by altering the gut microbiota through FMT and how these donor and recipient animals can be used to conduct controlled proof-of-principle “clinical” metagenomic studies of host-microbiome interrelations
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
