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Pasture Intake Protects Against Commercial Diet-induced Lipopolysaccharide Production Facilitated by Gut Microbiota through Activating Intestinal Alkaline Phosphatase Enzyme in Meat Geese

Published 29 Aug 2022 in q-bio.TO | (2208.13484v1)

Abstract: In-house feeding system (IHF, a low dietary fiber source) may cause altered cecal microbiota composition and inflammatory responses in meat geese via increased endotoxemia (lipopolysaccharides) with reduced intestinal alkaline phosphatase (ALP) production. The effects of artificial pasture grazing system (AGF, a high dietary fiber source) on modulating gut microbiota architecture and gut barrier functions have not been investigated in meat geese. The intestinal ALP functions to regulate gut microbial homeostasis and barrier function appears to inhibit pro-inflammatory cytokines by reducing LPS-induced reactive oxygen species (ROS) production. The purpose of our study was to investigate whether this enzyme could play a critical role in attenuating ROS generation and then ROS facilitated NF-\k{appa}B pathway-induced systemic inflammation in meat geese. First, we assessed the impacts of IHF and AGF on gut microbial composition via 16 sRNA sequencing in meat geese. In the gut microbiota analysis, meat geese supplemented with pasture demonstrated a significant reduction in microbial richness and diversity compared to IHF meat geese demonstrating antimicrobial, antioxidation, and anti-inflammatory ability of AGF system. Second host markers analysis through protein expression of serum and cecal tissues and quantitative PCR of cecal tissues were evaluated. We confirmed a significant increase in intestinal ALP-induced Nrf2 signaling pathway representing LPS dephosphorylation mediated TLR4/MyD88 induced ROS reduction mechanisms in AGF meat geese. Further, the correlation analysis of top 44 host markers with gut microbiota shows that artificial pasture intake induced gut barrier functions via reducing ROS-mediated NF-\k{appa}B pathway-induced gut permeability, systemic inflammation, and aging phenotypes.

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