Institute of Veterinary Physiology, Freie Universität Berlin, 14163 Berlin, Germany.
Institute of Animal Nutrition and Functional Plant Compounds, Department for Farm Animals and Veterinary Public Health, University of Veterinary Medicine Vienna, 1210 Vienna, Austria.
J Dairy Sci. 2019 Feb;102(2):1866-1882. doi: 10.3168/jds.2018-15243. Epub 2018 Dec 20.
The stratified squamous ruminal epithelium is the main site for absorption of key nutrients (e.g., short-chain fatty acids; SCFA) and electrolytes (e.g., sodium and magnesium). The absorptive function has to be highly selective to prevent simultaneous entry of microbes and toxins from the rumen into the blood. As such, epithelial absorption is primarily transcellular, whereas the paracellular pathway appears rather tightly sealed. A network of tight junction (claudin-1, claudin-4, and occludin) and tight junction-associated proteins (e.g., zonula occludens) accomplishes the latter. When microbial fermentation activity is high such as with highly fermentable diets, rumen epithelial functions are often challenged by acidity, high osmolarity, toxins (e.g., endotoxin and histamine), and immune mediators (inflammatory mediators and cytokines) released during local and systemic inflammation. Epithelial damage by low pH in combination with high luminal SCFA concentrations is not immediately reversible and may initially aggravate upon return to physiological pH. In contrast, barrier opening upon hyperosmolarity is acutely transient. The initial insults set by luminal acidity and SCFA and the increasing concentrations of microbial-associated molecular patterns such as lipopolysaccharides are key factors that trigger inflammation not only in the rumen but also in the hindgut (cecum and colon), which reach out to the liver and other organs, causing systemic inflammation. Low feed intake during parturition, transportation, heat stress, or disease is the second most relevant challenge for the ruminal epithelial barrier. The barrier opening is usually only transient and quickly restored upon refeeding. Due to a rapid, dose-dependent, and prolonged decrease in absorption capacity for SCFA, however, any feed restriction increases the odds for postrestriction subacute ruminal acidosis. Inflammation due to acidosis can be alleviated by supplemental thiamine, yeasts, and plant bioactive (phytogenic) compounds. Butyrate is used in weaning calves to support ruminal barrier development; however, excess butyrate may promote hyperkeratosis, parakeratosis, and epithelial injury in the fully developed rumen of adult cows. Further research is needed to enhance the understanding of the various factors that counteract barrier impairment and help barrier restoration during acidogenic feeding, especially when concurring with unavoidable periods of feed restriction.
复层鳞状的瘤胃上皮是吸收关键营养素（如短链脂肪酸；SCFA）和电解质（如钠和镁）的主要部位。吸收功能必须具有高度选择性，以防止同时从瘤胃进入血液的微生物和毒素进入。因此，上皮吸收主要是细胞间的，而细胞旁途径似乎被紧密密封。紧密连接（闭合蛋白 1、4 和紧密连接蛋白）和紧密连接相关蛋白（如闭合蛋白）的网络完成了后者。当微生物发酵活性很高，例如在高度可发酵的饮食中，瘤胃上皮功能经常受到酸度、高渗透压、毒素（如内毒素和组胺）和局部和全身炎症期间释放的免疫介质（炎症介质和细胞因子）的挑战。低 pH 值与高腔腔 SCFA 浓度相结合对上皮的损害不是立即可逆的，并且在返回生理 pH 值时最初可能会加剧。相比之下，高渗透压下的屏障打开是急性短暂的。腔腔酸度和 SCFA 的初始刺激以及微生物相关分子模式（如脂多糖）的浓度增加是不仅在瘤胃而且在后肠（盲肠和结肠）引发炎症的关键因素，这些炎症会扩散到肝脏和其他器官，导致全身性炎症。分娩、运输、热应激或疾病期间的低采食量是瘤胃上皮屏障的第二个最相关挑战。屏障打开通常只是短暂的，重新喂食后很快恢复。然而，由于 SCFA 吸收能力的快速、剂量依赖性和长期下降，任何饲料限制都会增加限制后亚急性瘤胃酸中毒的几率。酸中毒引起的炎症可以通过补充硫胺素、酵母和植物生物活性（植物源）化合物来缓解。然而，在完全发育的成年牛瘤胃中，丁酸过量可能会促进过度角化、角化不全和上皮损伤。需要进一步研究来增强对各种因素的理解，这些因素可以在产酸性喂养期间对抗屏障损伤并有助于屏障恢复，特别是在不可避免的饲料限制期间。
