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Intraruminal infusion of oligofructose alters ruminal microbiota and induces acute laminitis in sheep.

ABSTRACT: The objectives of this study were to examine the clinical response, changes in ruminal bacterial microbiota, and inflammatory response in lamellar tissues during oligofructose-induced laminitis. Ten fistulated sheep were randomly assigned into a control group ( = 5) and a treatment group ( = 5). The treatment group was infused with oligofructose (21 g/kg BW) by rumen cannula, and the control group was sham-treated with saline. Results showed that all 5 sheep treated with oligofructose developed anorexia and diarrhea 8 to 12 h after the administration of oligofructose. By 12 to 24 h after treatment, the treatment group developed lameness and roach back. Compared with the control group, oligofructose administration decreased ( < 0.001) the rumen pH and concentrations of total VFA and increased ( < 0.001) the level of lactic acid in the rumen. Microbial data analysis revealed that oligofructose infusion increased the abundance of ( = 0.009) and ( = 0.008) and decreased the percentage of unclassified Christensenellaceae ( = 0.028), unclassified Ruminococcaceae ( = 0.009), ( = 0.016), unclassified Lachnospiraceae ( = 0.009), and ( = 0.009) compared with the control group. Oligofructose infusion decreased the ACE ( = 0.047) and Shannon ( = 0.009) indices compared with the control group. The histomorphology analysis revealed that oligofructose overload resulted in damage to the dermoepidermal junction in the lamellar tissue of sheep. Quantitative real-time PCR results showed that compared with the control group, the mRNA expression of membrane-type metalloproteinase-1 ( = 0.049) was downregulated whereas the expression of proinflammatory IL-6 ( = 0.004) and matrix metalloprotease-9 ( = 0.037) was upregulated in the lamellar tissues of the oligofructose treatment group. In general, the present study provides the foundation for a sheep model of oligofructose-overload-induced acute laminitis that could be used in later experiments. Our findings suggest that intraruminal infusion of oligofructose altered ruminal microbiota and resulted in acute laminitis and that the inflammatory damage to the lamellae tissue may be related to the upregulation of matrix metalloprotease-9. The information generated will provide more insight into the systemic effects of lameness caused by oligofructose overload in sheep.

SUBMITTER: Li H

PROVIDER: S-EPMC6292330 | biostudies-literature | 2017 Dec

REPOSITORIES: biostudies-literature

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Intraruminal infusion of oligofructose alters ruminal microbiota and induces acute laminitis in sheep.

Li H H Liu J J Zhu W W Mao S S

Journal of animal science 20171201 12

The objectives of this study were to examine the clinical response, changes in ruminal bacterial microbiota, and inflammatory response in lamellar tissues during oligofructose-induced laminitis. Ten fistulated sheep were randomly assigned into a control group ( = 5) and a treatment group ( = 5). The treatment group was infused with oligofructose (21 g/kg BW) by rumen cannula, and the control group was sham-treated with saline. Results showed that all 5 sheep treated with oligofructose developed ...[more]

PMID: 29293794

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Project description:BackgroundUndernutrition is a prevalent and spontaneous condition in animal production which always affects microbiota-host interaction in gastrointestinal tract. However, how undernutrition affects crosstalk homeostasis is largely unknown. Here, we discover how undernutrition affects microbial profiles and subsequently how microbial metabolism affects the signal transduction and tissue renewal in ruminal epithelium, clarifying the detrimental effect of undernutrition on ruminal homeostasis in a pregnant sheep model.ResultsSixteen pregnant ewes (115 days of gestation) were randomly and equally assigned to the control (CON) and severe feed restriction (SFR) groups. Ewes on SFR treatment were restricted to a 30% level of ad libitum feed intake while the controls were fed normally. After 15 days, all ewes were slaughtered to collect ruminal digesta for 16S rRNA gene and metagenomic sequencing and ruminal epithelium for transcriptome sequencing. Results showed that SFR diminished the levels of ruminal volatile fatty acids and microbial proteins and repressed the length, width, and surface area of ruminal papillae. The 16S rRNA gene analysis indicated that SFR altered the relative abundance of ruminal bacterial community, showing decreased bacteria about saccharide degradation (Saccharofermentans and Ruminococcus) and propionate genesis (Succiniclasticum) but increased butyrate producers (Pseudobutyrivibrio and Papillibacter). Metagenome analysis displayed that genes related to amino acid metabolism, acetate genesis, and succinate-pathway propionate production were downregulated upon SFR, while genes involved in butyrate and methane genesis and acrylate-pathway propionate production were upregulated. Transcriptome and real-time PCR analysis of ruminal epithelium showed that downregulated collagen synthesis upon SFR lowered extracellular matrix-receptor interaction, inactivated JAK3-STAT2 signaling pathway, and inhibited DNA replication and cell cycle.ConclusionsGenerally, undernutrition altered rumen bacterial community and function profile to decrease ruminal energy retention, promoted epithelial glucose and fatty acid catabolism to elevate energy supply, and inhibited the proliferation of ruminal epithelial cells. These findings provide the first insight into the systemic microbiota-host interactions that are involved in disrupting the ruminal homeostasis under a malnutrition pattern. Video Abstract.

Project description:The demand for economic benefits has led to an increase in the proportion of high-concentrate (HC) feed in the ruminant diet, resulting in an increased incidence of subacute ruminal acidosis (SARA). During SARA, a high concentration of lipopolysaccharide (LPS) translocated in the rumen induces a systemic inflammatory response. Inflammatory diseases, such as endometritis and mastitis, are often associated with SARA; however, in sheep, the mechanism of the effect of SARA on the endometrium has rarely been reported. Therefore, the aim of this study was to investigate, for the first time, the influence of LPS translocation on endometrial tight junctions (TJs) during SARA in sheep. The results showed that LPS and TNFα levels in the ruminal fluid, serum, and endometrial tissue supernatant during SARA increased, transcription levels of TLR4, NFκB, and TNFα in the endometrium increased, the protein expression level of claudin-1 in the endometrium increased, and the protein expression level of occludin decreased. 17β-estradiol (E2) inhibits claudin-1 protein expression and promotes occludin expression, and progesterone (P4) promotes claudin-1 protein expression and inhibits occludin protein expression. E2 and P4 regulate claudin-1 and occludin protein expression through their receptor pathways. Here, we found that LPS hindered the regulatory effect of E2 and P4 on endometrial TJs by inhibiting their receptor expression. The results of this study indicate that HC feeding can cause SARA-induced LPS translocation in sheep, increase susceptibility to systemic inflammation, induce the endometrial inflammatory response, and cause endometrial epithelial TJ damage directly and/or by obstructing E2 and P4 function. LPS translocation caused by SARA has also been suggested to induce an endometrial inflammatory response, resulting in endometrial epithelial barrier damage and physiological dysfunction, which seriously affects ruminant production. Therefore, this study provides new evidence that SARA is a potential factor that induces systemic inflammation in ruminants. It provides theoretical support for research on the prevention of endometritis in ruminants.

Project description:Bovine laminitis leads to huge economic losses and animal welfare problems in the dairy industry worldwide. Numerous studies suggested that several metalloproteinases (MPs) may play vital roles in the failure of epidermal attachment. To the best of our knowledge, the present study is the first to investigate and characterize the gene-level changes in distinct MPs and endogenous inhibitors using oligofructose (OF)-induced bovine laminitis model. The objective of this study was to determine aberrant MPs and related inhibitors of bovine laminitis in gene level, and to provide reasonable directions for the further protein-level research. Twelve normal Chinese Holstein dairy heifers were randomly divided into treatment group (n = 6) and control group (n = 6). The heifers in the treatment group were administered with OF solutions at a dose of 17 g/kg of body weight via a stomach tube. The heifers were then humanely euthanized when they met the criteria of bovine laminitis. The heifers in the control group were administered with deionized water at a dose of 2 L/100 kg of body weight. They humanely euthanized at 72 h. The gene expressions of MPs and endogenous inhibitors, namely, matrix metalloproteinases (MMPs), A disintegrin and metalloproteinases (ADAMs), and A disintegrin and metalloproteinase with thrombospondin motifs (ADAMTs), and tissue inhibitors of metalloproteinases (TIMPs) in the lamellae from two groups were determined via real-time quantitative PCR. The gene expressions of MMP-2, MMP-9, ADAMTS-4, and ADAMTS-5 significantly increased (P < 0.05), whereas that of TIMP-2 significantly decreased (P < 0.05) in the treatment group relative to the control group. No significant difference was found in the gene expressions of ADAM-10, ADAM-17, TIMP-1, and TIMP-3. These results indicated that the gene-level imbalanced condition of MPs and their TIMPs may be the basic cause for the failure of epidermal attachment. At the same time, more detailed protein-level studies would be needed to further clarify the roles of MPs and TIMPs in the pathogenesis of bovine laminitis, especially to MMP-2, MMP-9, ADAMTS-4, ADAMTS-5, TIMP-2 as well as related substrates (e.g., aggrecan and versican).

Dataset Information

Intraruminal infusion of oligofructose alters ruminal microbiota and induces acute laminitis in sheep.

Publications

Intraruminal infusion of oligofructose alters ruminal microbiota and induces acute laminitis in sheep.

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