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Impacts of Ruminal Acidosis on Animal Health and Performance

机译：瘤胃酸中毒对动物健康和生产性能的影响

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Subacute Ruminal Acidosis (SARA) resulting from a grain overload has been associated with increases of lipopolysaccharide (LPS) in digesta and blood,as well as signs of inflammation,such as an acute phase response.This response is part of the innate immune system and is characterized by elevated levels ofserum amyloid A (SAA),haptoglobin (Hp),and LPS binding protein (LBP)in the blood.Production of these acute phase proteins is driven by a variety of cytokines that include interleukin 6 (IL-6),tumor necrosis factor α (TNFαt).It is assumed that the production of these cytokines is activated when LPS-LBP complexes bind with toll-like receptors (TLR),such as TLR-4.Intravenous administration of LPS derived from E.colicause log-fold rises of SAA,HP,LBP,IL-6 and TNFαt in blood plasma,as well as fever and a leukocyte count response.It has become clear that LPS needs to translocate through the epithelium of the digestive tract in order to activate TLR.Detection of LPS in peripheral bloodand a reduction of the barrier function of the epithelia of the rumenand the large intestine,suggest that this translocation may occur during SARA.However,these studies have not been able to identify the sites through which LPS or other immunogenic compounds may betranslocated.Gross anatomical and histological differences in the epithelium of the rumen and the large intestine suggest that hindgut acidosis may create a greater risk for LPS translocation than rumen acidosis.Measurement of LPS in the blood of cows during SARA suggests that the amount of LPS that is translocated during SARA is similar to the doses that have been used during studies in which E.coli LPS was administered intravenously to cows.In contrast to intravenous injection of LPS,experimentally induced SARA is generally not associated with fever,changes in leucocyte count,or massive increases in acute phase proteins and cytokines.One reason for this discrepancy may be that the toxicity of enteric LPS from cattle may be lower than that from the E.coli that was administered intravenously.Another reason for this discrepancy may be an endotoxin tolerance that is developed by continuous exposure to LPS during SARA and that is not developed during a one-time intravenous administration of LPS.The mechanism behind tolerance to repeated exposure to LPS is not yet well understood.A better understanding of this mechanism will contribute to strategies that enhance health and welfare of ruminants on high grain diets.
机译：谷物超负荷导致的亚急性瘤胃酸中毒（SARA）与消化系统和血液中脂多糖（LPS）的增加以及炎症迹象（例如急性期反应）有关。这种反应是先天免疫系统和免疫系统的一部分。其特征是血液中的血清淀粉样蛋白A（SAA），触珠蛋白（Hp）和LPS结合蛋白（LBP）升高。这些急性期蛋白的产生受多种细胞因子驱动，包括白介素6（IL-6） LPS-肿瘤坏死因子α（TNFαt）。假定当LPS-LBP复合物与toll样受体（TLR）（例如TLR-4）结合时，这些细胞因子的产生被激活。静脉注射源自大肠杆菌的LPS血浆中SAA，HP，LBP，IL-6和TNFαt的对数升高，以及发烧和白细胞计数反应。很明显，LPS需要转运通过消化道上皮才能激活TLR。外周血中脂多糖的检测瘤胃和大肠上皮屏障功能的产生，提示这种移位可能发生在SARA期间。但是，这些研究未能确定LPS或其他免疫原性化合物可以移位的部位。瘤胃上皮和大肠上皮的差异表明，后肠酸中毒可能比瘤胃酸中毒产生更大的脂多糖易位风险。在SARA期间奶牛血液中LPS的测定表明，SARA期间脂蛋白的易位量相似与向牛静脉内施用LPS的研究剂量相同。与LPS静脉注射相反，实验诱导的SARA通常与发烧，白细胞计数变化或急性期大量增加无关。这种差异的一个原因可能是牛肠道LPS的毒性可能较低另一个原因可能是内毒素耐受性，它是在SARA期间持续暴露于LPS而形成的，而不是在一次静脉内施用LPS时产生的。反复暴露于LPS的耐受性尚未得到很好的理解。对此机制的更好理解将有助于提高高谷物饮食反刍动物的健康和福利的策略。

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