Mordak Ryszard, Stewart Peter Anthony
Department of Internal Medicine and Clinic of Diseases of Horses, Dogs and Cats, Faculty of Veterinary Medicine, Wrocław University of Environmental and Life Sciences, Grunwaldzki Sq. 47, 50-366, Wrocław, Poland.
Veterinary Clinic Stewart and Partners, 2 Brooke Street, Dudley, DY2 8RB, UK.
Acta Vet Scand. 2015 Dec 2;57:84. doi: 10.1186/s13028-015-0175-2.
The immune system during the periparturient period is impaired. At this time the most important factor causing immune-suppression in highly productive cows is metabolic stress resulting from hormonal and metabolic fluctuations, a negative energy balance, shortage of proteins, minerals and vitamins which are required to meet the demands of the fetus as well as the onset of lactation. This stress can activate the hypothalamic-pituitary-adrenocortical axis (HPA), which results in increase plasma corticosteroids. As a result, the cortisol concentration during the periparturient period increases by several folds particularly on the day of calving. Cortisol is a powerful immune-suppressive agent. During stress, this hormone causes depression of the leukocyte proliferation and their functions. Decreased phagocytosis of neutrophils, decreased cytotoxic ability of lymphocytes, as well as depressed activity of their cytokines, make it impossible for the normal, efficient maternal immune recognition and rejection of fetal membranes (as a foreign, allogeneic tissue expressed fetal antigens-MHC class I proteins by trophoblast cells) and finally results in their retention in cows. The metabolic periparturient stress also activates production of catecholamines, especially adrenalin. Adrenalin activates adrenoreceptors of the myometrium and then causes hypotony or atony of the uterus. Thus, cortisol and adrenalin inhibit rejection and expulsion of fetal membranes and cause their retention. These mechanisms of retained placenta (RP) often have a metabolic etiology and occur in herds, where important infectious diseases causing placentitis are absent or prevented. The aim of this article is to show the fundamental mechanisms occurring during periparturient stress and the accompanied immune-suppression in cows, as well as their consequences in relation to RP. The paper also gives examples of the symptomatic prevention of RP in cows caused by metabolic and immune suppressive factors. The prevention of RP was carried out using drugs which inhibit the activity of cortisol or adrenalin in dairy cows during calving.
围产期的免疫系统会受到损害。此时，导致高产奶牛免疫抑制的最重要因素是激素和代谢波动、负能量平衡、蛋白质、矿物质和维生素短缺所引起的代谢应激，这些都是满足胎儿需求以及泌乳开始所必需的。这种应激会激活下丘脑 - 垂体 - 肾上腺皮质轴（HPA），导致血浆皮质类固醇增加。结果，围产期的皮质醇浓度会增加数倍，尤其是在产犊当天。皮质醇是一种强大的免疫抑制剂。在应激期间，这种激素会导致白细胞增殖及其功能受到抑制。中性粒细胞吞噬作用降低、淋巴细胞细胞毒性能力下降以及它们的细胞因子活性受到抑制，使得母体无法正常、有效地识别和排斥胎膜（作为一种由滋养层细胞表达胎儿抗原 - MHC I类蛋白的外来、同种异体组织），最终导致胎膜在奶牛体内滞留。围产期的代谢应激还会激活儿茶酚胺的产生，尤其是肾上腺素。肾上腺素激活子宫肌层的肾上腺素能受体，进而导致子宫张力减退或弛缓。因此，皮质醇和肾上腺素会抑制胎膜的排斥和排出，导致胎膜滞留。这些胎盘滞留（RP）的机制通常具有代谢病因，并且发生在不存在或已预防引起胎盘炎的重要传染病的牛群中。本文的目的是展示奶牛围产期应激期间发生的基本机制以及伴随的免疫抑制，以及它们与胎盘滞留的关系。本文还给出了由代谢和免疫抑制因素引起的奶牛胎盘滞留的症状性预防示例。通过在奶牛产犊期间使用抑制皮质醇或肾上腺素活性的药物来预防胎盘滞留。
