Gholizade M, Fayazi J, Zali H, Asgari Y
Department of Animal Sciences, Faculty of Animal Sciences and Food technology, Agricultural Sciences and Natural Resources University of Khuzestan, Mollasani, Ahvaz, Iran.
Department of Tissue Engineering and Applied Cell Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Arch Razi Inst. 2020 Mar;75(1):109-121. doi: 10.22092/ari.2019.125930.1326. Epub 2020 Mar 1.
The transition from normal forage to a highly fermentable diet to achieve rapid weight gain in the cattle industry can induce ruminal acidosis. The molecular host mechanisms that occur in acidosis are largely unknown. Therefore, the histology and transcriptome profiling of rumen epithelium was investigated in normal and acidosis animals to understand the molecular mechanisms involved in the disease. The rumen epithelial transcriptome from acidosis (n=3) and control (n=3) Holstein steers was obtained using RNA-sequencing. The mean values of clean reads were 70,975,460±984,046 and 71,142,189±834,526 in normal and acidosis samples, respectively. In total, 1,074 differentially expressed genes were identified in the two groups (P<0.05), of which 624 and 450 genes were up- and down-regulated in the acidosis samples, respectively. Functional analysis indicated that the majority of the up-regulated genes had a function in filament organization, positive regulation of epithelial and muscle fiber concentration, biomineral tissue development, negative regulation of fat cell differential, regulation of ion transmembrane transport, regulation of cell adhesion and butyrate, as well as short-chain fatty acid absorption that was metabolized as an energy source. Functional analysis of the down-regulated genes revealed effects in immune response, positive regulation of T-cell migration, regulation of metabolic processes, and localization. Furthermore, the results showed a differential expression of genes involved in the Map Kinase and Toll-like receptor signaling pathways. The IL1B, CXCL5, IL36A, and IL36B were significantly down-regulated in acidosis rumen tissue samples. The results suggest that rapid shifts to rich fermentable carbohydrates diets cause an increase in the concentration of ruminal volatile fatty acids, tissue damage, and significant changes in transcriptome profiles of rumen epithelial.
在养牛业中,从正常草料过渡到高发酵性日粮以实现快速增重,可能会引发瘤胃酸中毒。酸中毒时发生的分子宿主机制在很大程度上尚不清楚。因此,对正常和酸中毒动物的瘤胃上皮进行组织学和转录组分析,以了解该疾病涉及的分子机制。使用RNA测序获得了酸中毒(n = 3)和对照(n = 3)荷斯坦公牛的瘤胃上皮转录组。正常和酸中毒样本中,clean reads的平均值分别为70,975,460±984,046和71,142,189±834,526。两组共鉴定出1074个差异表达基因(P<0.05),其中酸中毒样本中分别有624个和450个基因上调和下调。功能分析表明,大多数上调基因在细丝组织、上皮和肌纤维浓度的正调控、生物矿化组织发育、脂肪细胞分化的负调控、离子跨膜转运调控、细胞粘附调控以及丁酸和短链脂肪酸吸收(作为能量来源进行代谢)方面具有功能。下调基因的功能分析显示在免疫反应、T细胞迁移的正调控、代谢过程调控和定位方面有影响。此外,结果显示参与丝裂原活化蛋白激酶(Map Kinase)和Toll样受体信号通路的基因存在差异表达。IL1B、CXCL5、IL36A和IL36B在酸中毒瘤胃组织样本中显著下调。结果表明,迅速转向富含可发酵碳水化合物的日粮会导致瘤胃挥发性脂肪酸浓度增加、组织损伤以及瘤胃上皮转录组谱的显著变化。