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Xylooligosaccharide attenuates lipopolysaccharide-induced intestinal injury in piglets via suppressing inflammation and modulating cecal microbial communities

机译:含有抑制炎症和调节盲肠微生物群落的仔猪在仔猪中衰减脂多糖诱导的血液多糖诱导的肠损伤

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Xylooligosaccharide (XOS) has been considered to be an effective prebiotic, but its exact mechanisms remain unknown. This research was conducted to evaluate the effects of XOS on pig intestinal bacterial community and mucosal barrier using a lipopolysaccharide (LPS)-caused gut damage model. Twenty-four weaned pigs were assigned to 4 treatments in a 2?×?2 factorial design involving diet (with or without XOS) and immunological challenge (saline or LPS). After 21?d of feeding 0% or 0.02% commercial XOS product, piglets were treated with saline or LPS. After that, blood, small intestinal mucosa and cecal digesta were obtained. Dietary XOS enhanced intestinal mucosal integrity demonstrated by higher villus height, villus height-to-crypt depth ratio, disaccharidase activities and claudin-1 protein expression and lower crypt depth. XOS also caused down-regulation of the gene expression of toll-like receptor 4 and nucleotide-binding oligomerization domain protein signaling, accompanied with decreased pro-inflammatory cytokines and cyclooxygenase 2 contents or mRNA expression and increased heat shock protein 70?mRNA and protein expression. Additionally, increased Bacteroidetes and decreased Firmicutes relative abundance were observed in the piglets fed with XOS. At the genus level, XOS enriched the relative abundance of beneficial bacteria, e.g., Faecalibacterium , Lactobacillus , and Prevotella . Moreover, XOS enhanced short chain fatty acids contents and inhibited histone deacetylases. The correlation analysis of the combined datasets implied some potential connections between the intestinal microbiota and pro-inflammatory cytokines or cecal metabolites. These results suggest that XOS inhibits inflammatory response and beneficially modifies microbes and metabolites of the hindgut to protect the intestine from inflammation-related injury.
机译:甲洛尼糖(XOS)被认为是一种有效的益生元,但其确切的机制仍然未知。进行了该研究以评估XOS对猪肠道细菌群落和粘膜屏障的影响使用脂多糖(LPS)-COUSED GUT损伤模型。将24只断奶猪分配到4次涉及饮食(有或没有XOS)和免疫攻击(盐水或LPS)的4次治疗。在喂养0%或0.02%商业XOS产品的21℃后,用盐水或LPS处理仔猪。之后,获得血液,小肠粘膜和盲肠粘膜。膳食XOS增强肠粘膜完整性,绒毛高度较高,绒毛高度到穴位比例,失空酶活性和克劳德蛋白-1蛋白表达和较低的穴位深度。 XOS还引起了伴随收缩受体4的基因表达和核苷酸结合寡聚化结构域蛋白质信号传导,伴随着降低的促炎细胞因子和环氧化酶2含量或mRNA表达和增加的热休克蛋白70?mRNA和蛋白质表达增加。另外,在用XOS供给的仔猪中观察到增加的菌体和降低的相对丰度。在Genus水平,XOS富集了有益细菌的相对丰富,例如,粪便杆菌,乳酸杆菌和PREVotella。此外,XOS增强的短链脂肪酸含量和抑制组蛋白脱乙酰酶。组合数据集的相关性分析暗示肠道微生物群和促炎细胞因子或肠代谢物之间的一些潜在连接。这些结果表明XOS抑制炎症反应,有利地改变后肠的微生物和代谢物,以保护肠免受炎症相关的损伤。

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