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

Abstract

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.

Ellagic Acid Alleviates Oxidative Stress by Mediating Nrf2 Signaling Pathways and Protects against Paraquat-Induced Intestinal Injury in Piglets

“…In the present study, we also observed that EA administrations alleviated microvilli shedding and crypt hyperplasia, as well as increased the number of goblet cells in piglets injected with PQ, which is consistent with previous studies [ 51 ]. Oxidative stress can cause the intestinal barrier injury mainly manifested as villi shorting, crypt hyperplasia, and goblet cells apoptosis, which contribute further to a reduced ability for nutritional absorption and presentation of pathogens [ 62 , 63 ]. Maintaining intestinal integrity is a prerequisite to ensure the intestinal barrier function [ 64 ].…”

The Multi-Omics Analysis Revealed Microbiological Regulation of Rabbit Colon with Diarrhea Fed an Antibiotic-Free Diet

“…The diversity and evenness of microorganisms in the DIA group decreased significantly, while Bacteroidetes increased significantly and Firmicutes decreased significantly. The ratio of Firmicutes and Bacteroidetes could often reflect the health situation in the colon [ 24 , 25 ]. In healthy individuals, the index of Firmicutes / Bacteroidetes (F/B > 1) is usually high, and an imbalance in the F/B index can lead to an inflammatory response [ 26 , 27 ].…”

Protective Effects of a Novel Probiotic Bifidobacterium pseudolongum on the Intestinal Barrier of Colitis Mice via Modulating the Pparγ/STAT3 Pathway and Intestinal Microbiota

“…Histopathological examination of colon tissues was carried out as reported previously [ 9 ]. Briefly, the colons were removed, fixed, and embedded in paraffin.…”

“…Immunohistochemical analysis was carried out following our previous study [ 9 ]. Briefly, the sections of the colon were incubated with primary antibodies specific to occludin (Abcam, ab216327), claudin-1 (Abcam, ab180158), and ZO-1 (Abcam, ab221546) for 60 min, followed by incubation with secondary antibody and streptavidin-biotin peroxidase for 120 min.…”

“…Increases in harmful bacteria elevate the probability of direct interaction between the microbes and host tissue, thereby accelerating the occurrence and development of IBD. Moreover, recent reports have shown that an imbalance of the intestinal microbiota not only destroys the intestinal barrier via increasing the expression of MyD88 but also promotes the release of pro-inflammatory cytokines via activating the NF-κB pathway [ 9 ]. Hence, maintaining a healthy balance of intestinal microbiota is important for preventing or/and treating IBD.…”