The Cell Wall Utilization and Biology Laboratory, US Dairy Forage Research Center, USDA ARS, Madison, WI, 53706, USA.
Department of Dairy Science, University of Wisconsin-Madison, Madison, WI, 53706, USA.
Sci Rep. 2019 Mar 18;9(1):4744. doi: 10.1038/s41598-019-40375-2.
Many common management practices used to raise dairy calves while on milk and during weaning can cause rumen acidosis. Ruminal pH has long been used to identify ruminal acidosis. However, few attempts were undertaken to understand the role of prolonged ruminal acidosis on rumen microbial community or host health in young calves long after weaning. Thus, the molecular changes associated with prolonged rumen acidosis in post weaning young calves are largely unknown. In this study, we induced ruminal acidosis by feeding a highly processed, starch-rich diet to calves starting from one week of age through 16 weeks. Rumen epithelial tissues were collected at necropsy at 17 weeks of age. Transcriptome analyses on the rumen epithelium and meta-transcriptome analysis of rumen epimural microbial communities were carried out. Calves with induced ruminal acidosis showed significantly less weight gain over the course of the experiment, in addition to substantially lower ruminal pH in comparison to the control group. For rumen epithelial transcriptome, a total of 672 genes (fold-change, FC ≥ 1.5; adjusted-p ≤ 0.05) showed significant differential expression in comparison to control. Biological pathways impacted by these differentially expressed genes included cell signaling and morphogenesis, indicating the impact of ruminal acidosis on rumen epithelium development. rRNA read-based microbial classification indicated significant increase in abundance of several genera in calves with induced acidosis. Our study provides insight into host rumen transcriptome changes associated with prolonged acidosis in post weaning calves. Shifts in microbial species abundance are promising for microbial species-based biomarker development and artificial manipulation. Such knowledge provides a foundation for future more precise diagnosis and preventative management of rumen acidosis in dairy calves.
许多用于提高哺乳期和断奶期奶牛犊牛的常见管理实践都会导致瘤胃酸中毒。瘤胃 pH 值长期以来一直用于识别瘤胃酸中毒。然而，很少有人试图了解断奶后很长一段时间内，慢性瘤胃酸中毒对小牛瘤胃微生物群落或宿主健康的影响。因此，在断奶后不久的小牛中，与慢性瘤胃酸中毒相关的分子变化在很大程度上仍不清楚。在这项研究中，我们从一周龄开始通过给小牛喂食高度加工的富含淀粉的饮食来诱导瘤胃酸中毒，并持续到 16 周。在 17 周龄进行尸检时收集瘤胃上皮组织。对瘤胃上皮组织进行转录组分析，并对瘤胃上皮外微生物群落进行元转录组分析。与对照组相比，诱导瘤胃酸中毒的小牛在整个实验过程中体重增加明显较少，瘤胃 pH 值也明显较低。对于瘤胃上皮转录组，与对照组相比，共有 672 个基因（倍数变化，FC≥1.5；调整后 p 值≤0.05）表现出显著差异表达。受这些差异表达基因影响的生物途径包括细胞信号转导和形态发生，表明瘤胃酸中毒对瘤胃上皮发育的影响。rRNA 读码微生物分类表明，诱导酸中毒的小牛中几种属的丰度显著增加。我们的研究提供了宿主瘤胃转录组与断奶后小牛慢性酸中毒相关变化的见解。微生物物种丰度的变化有望为基于微生物物种的生物标志物开发和人工操作提供依据。这些知识为未来更精确地诊断和预防奶牛犊牛瘤胃酸中毒提供了基础。
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