Intraruminal infusion of oligofructose alters ruminal microbiota and induces acute laminitis in sheep
Intraruminal infusion of oligofructose alters ruminal microbiota and induces acute laminitis in sheep
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瘤胃内输注低聚果糖会改变绵羊瘤胃微生物群并诱发急性蹄叶炎
DOI：
10.2527/jas2017.1860
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发表时间：
2017-12-01
影响因子：
3.3
通讯作者：
Mao, S.
中科院分区：
文献类型：
--
作者：
Li, H.;Liu, J.;Mao, S.
本研究的目的是检查临床反应，瘤胃细菌微生物群的变化，以及在板层组织中的炎症反应，在寡果糖诱导的蹄叶炎。将10只瘘管绵羊随机分为对照组（n = 5）和治疗组（n = 5）。治疗组经瘤胃套管注入低聚果糖（21 g/kg BW），对照组注入生理盐水。结果表明，低聚果糖组的5只绵羊均在给药后8 ~ 12 h出现厌食和腹泻。给药后12 ~ 24 h，治疗组出现跛行和蟑螂背部。与对照组相比，低聚果糖显著降低瘤胃pH值和总VFA浓度（P < 0.001），显著提高瘤胃乳酸水平（P < 0.001）。微生物数据分析显示，低聚果糖输注增加了链球菌的丰度（P = 0.009）和乳酸菌（P = 0.008），降低了未分类的Christensenellaceae的百分比（P = 0.028），未分类瘤胃球菌科（P = 0.009）、丁酸弧菌（P = 0.016）、未分类毛螺菌科（P = 0.009）和瘤胃球菌（P = 0.009）。与对照组相比，低聚果糖输注降低了ACE（P = 0.047）和Shannon（P = 0.009）指数。组织形态学分析表明，低聚果糖负荷导致绵羊板层组织真皮表皮连接处的损伤。实时荧光定量PCR结果显示，与对照组相比，低聚果糖治疗组板层组织中膜型金属蛋白酶-1（P = 0.049）的mRNA表达下调，而促炎因子IL-6（P = 0.004）和基质金属蛋白酶-9（P = 0.037）的表达上调。总的来说，本研究提供了基础的绵羊模型寡果糖超载诱导的急性蹄叶炎，可用于以后的实验。我们的研究结果表明，低聚果糖的瘤胃内输注改变了瘤胃微生物群，并导致急性蹄叶炎，蹄叶组织的炎性损伤可能与基质金属蛋白酶-9的上调有关。所产生的信息将提供更多的洞察力跛行引起的低聚果糖过载在绵羊的全身影响。
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 (n = 5) and a treatment group (n = 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 (P < 0.001) the rumen pH and concentrations of total VFA and increased (P < 0.001) the level of lactic acid in the rumen. Microbial data analysis revealed that oligofructose infusion increased the abundance of Streptococcus (P = 0.009) and Lactobacillus (P = 0.008) and decreased the percentage of unclassified Christensenellaceae (P = 0.028), unclassified Ruminococcaceae (P = 0.009), Butyrivibrio (P = 0.016), unclassified Lachnospiraceae (P = 0.009), and Ruminococcus (P = 0.009) compared with the control group. Oligofructose infusion decreased the ACE (P = 0.047) and Shannon (P = 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 (P = 0.049) was downregulated whereas the expression of proinflammatory IL-6 (P = 0.004) and matrix metalloprotease-9 (P = 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.