Department of Animal Science, Iowa State University, Ames 50011, USA.
J Anim Sci. 2012 May;90(5):1452-65. doi: 10.2527/jas.2011-4627. Epub 2012 Jan 13.
Endotoxin, also referred to as lipopolysaccharide (LPS), can stimulate localized or systemic inflammation via the activation of pattern recognition receptors. Additionally, endotoxin and inflammation can regulate intestinal epithelial function by altering integrity, nutrient transport, and utilization. The gastrointestinal tract is a large reservoir of both gram-positive and gram-negative bacteria, of which the gram-negative bacteria serve as a source of endotoxin. Luminal endotoxin can enter circulation via two routes: 1) nonspecific paracellular transport through epithelial cell tight junctions, and 2) transcellular transport through lipid raft membrane domains involving receptor-mediated endocytosis. Paracellular transport of endotoxin occurs through dissociation of tight junction protein complexes resulting in reduced intestinal barrier integrity, which can be a result of enteric disease, inflammation, or environmental and metabolic stress. Transcellular transport, via specialized membrane regions rich in glycolipids, sphingolipids, cholesterol, and saturated fatty acids, is a result of raft recruitment of endotoxin-related signaling proteins leading to endotoxin signaling and endocytosis. Both transport routes and sensitivity to endotoxin may be altered by diet and environmental and metabolic stresses. Intestinal-derived endotoxin and inflammation result in suppressed appetite, activation of the immune system, and partitioning of energy and nutrients away from growth toward supporting the immune system requirements. In livestock, this leads to the suppression of growth, particularly suppression of lean tissue accretion. In this paper, we summarize the evidence that intestinal transport of endotoxin and the subsequent inflammation leads to decrease in the production performance of agricultural animals and we present an overview of endotoxin detoxification mechanisms in livestock.
内毒素，也称为脂多糖（LPS），可以通过激活模式识别受体来刺激局部或全身炎症。此外，内毒素和炎症可以通过改变完整性、营养物质运输和利用来调节肠道上皮细胞功能。胃肠道是革兰氏阳性和革兰氏阴性细菌的巨大储库，其中革兰氏阴性细菌是内毒素的来源。内毒素可以通过两种途径进入循环：1）通过上皮细胞紧密连接的非特异性旁细胞转运，2）通过涉及受体介导的内吞作用的质膜域的跨细胞转运。内毒素的旁细胞转运是通过紧密连接蛋白复合物的解离发生的，导致肠道屏障完整性降低，这可能是肠道疾病、炎症或环境和代谢应激的结果。通过富含糖脂、鞘脂、胆固醇和饱和脂肪酸的特殊膜区域的跨细胞转运是由于内毒素相关信号蛋白募集到筏上，导致内毒素信号和内吞作用。两种转运途径和对内毒素的敏感性都可能受到饮食、环境和代谢应激的影响。肠道来源的内毒素和炎症导致食欲下降、免疫系统激活，并将能量和营养物质从生长分配到支持免疫系统需求。在牲畜中，这会导致生长抑制，特别是瘦肉组织积累的抑制。本文总结了肠道内毒素转运和随后的炎症导致农业动物生产性能下降的证据，并概述了牲畜内毒素解毒机制。
