Acute and subacute ruminal acidosis (SARA) are common nutritional problems in both beef and dairy cattle. Therefore, the objective of this review is to describe how ruminal Gram-negative bacteria could contribute to the pathogenesis of ruminal acidosis, by releasing lipopolysaccharides (LPS; a component of their cell-wall) in the ruminal fluid. When cattle consume excessive amounts of highly fermentable carbohydrates without prior adaptation, normal fermentation become disrupted. The fermentation of these carbohydrates quickly decreases ruminal pH due to the accumulation of short-chain fatty acids (SCFA) and lactate in the rumen. As a consequence, ruminal epithelium may be damaged and tissue function could be impaired, leading to a possible translocation of pathogenic substances from the rumen into the blood stream. Such changes in fermentation are followed by an increase in Gram-positive bacteria while Gram-negative bacteria decrease. The lyses of Gram-negative bacteria during ruminal acidosis increase LPS concentration in the ruminal fluid. Because LPS is a highly pro-inflammatory endotoxin in the circulatory system, past studies have raised concerns regarding ruminal LPS contribution to the pathogenesis of ruminal acidosis. Although animals that undergo these disorders do not always have an immune response, recent studies showed that different Gram-negative bacteria have different LPS composition and toxicity, which may explain the differences in immune response. Given the diversity of Gram-negative bacteria in the rumen, evaluating the changes in bacterial community during ruminal acidosis could be used as a way to identify which Gram-negative bacteria are associated with LPS release in the rumen. By identifying and targeting ruminal bacteria with possible pathogenic LPS, nutritional strategies could be created to overcome, or at least minimize, ruminal acidosis.

中文翻译：

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瘤胃酸中毒、细菌变化和脂多糖。

急性和亚急性瘤胃酸中毒 (SARA) 是肉牛和奶牛常见的营养问题。因此，本综述的目的是描述瘤胃革兰氏阴性菌如何通过在瘤胃液中释放脂多糖（LPS；其细胞壁的一种成分）而促进瘤胃酸中毒的发病机制。当牛在没有事先适应的情况下食用过量的高度可发酵的碳水化合物时，正常的发酵就会被破坏。由于短链脂肪酸 (SCFA) 和乳酸在瘤胃中的积累，这些碳水化合物的发酵会迅速降低瘤胃的 pH 值。因此，瘤胃上皮可能受损，组织功能可能受损，导致病原物质可能从瘤胃转移到血流中。发酵过程中发生这种变化后，革兰氏阳性菌增多，而革兰氏阴性菌减少。瘤胃酸中毒期间革兰氏阴性菌的裂解增加了瘤胃液中的 LPS 浓度。由于 LPS 是循环系统中一种高度促炎的内毒素，过去的研究引起了对瘤胃 LPS 对瘤胃酸中毒发病机制的影响的担忧。尽管患有这些疾病的动物并不总是有免疫反应，但最近的研究表明，不同的革兰氏阴性菌具有不同的 LPS 成分和毒性，这可能解释了免疫反应的差异。鉴于瘤胃中革兰氏阴性菌的多样性，评估瘤胃酸中毒期间细菌群落的变化可用作确定哪些革兰氏阴性菌与瘤胃中 LPS 释放相关的方法。通过识别和靶向可能具有致病性 LPS 的瘤胃细菌，可以制定营养策略来克服或至少减少瘤胃酸中毒。