Shuster D E, Kehrli M E, Baumrucker C R
Department of Metabolic Disease and Immunology, U.S. Department of Agriculture-Agricultural Research Service, Ames, Iowa 50010, USA.
Proc Soc Exp Biol Med. 1995 Nov;210(2):140-9. doi: 10.3181/00379727-210-43933.
Production of inflammatory cytokines and concentrations of growth hormone and insulin-like growth factor-I (IGF-I) were studied during experimental Escherichia coli mastitis to determine their potential involvement in reduced animal performance during infectious disease. During the first 10 to 14 hr after intramammary infusion of E. coli, bacteria multiplied to maximum levels of 10(4)-10(9) cfu/ml of milk with no clinical signs of mastitis. A rapid and intense inflammatory response, characterized by udder swelling, increased bovine serum albumin (BSA) and somatic cell count (SCC) in milk of infected glands, and elevated rectal temperature and serum cortisol concentration, began at approximately 12 hr after challenge. Lactational performance was reduced greatly at 24 hr, and the maximal decrease averaged 76% and 63% among infected and uninfected glands, respectively, of challenged cows; three cows became temporarily agalactic in all glands. By 6 days, all cows had nearly or completely eliminated the E. coli, and milk production had partially recovered. Milk composition showed an initial decrease in fat percentage followed by an increase thereafter. Protein percentage was increased and lactose content was reduced during most of the mastitic episode. High concentrations of tumor necrosis factor (TNF) and interleukin-1 (IL-1) were detected in milk of infected glands, and their appearance preceded or coincided with development of the mammary inflammation, systemic reaction, and hypogalactia. Serum growth hormone concentration was higher among challenged cows, whereas serum IGF-I concentrations changed little during the mastitic episode. Concentrations of IGF-I in milk whey increased from 5.0 to 12.2 ng/ml among infected glands and from 4.4 to 8.5 ng/ml among contralateral, uninfected glands; IGF binding proteins also increased in the milk of infected glands. These data demonstrate that (i) reduced lactational performance is not caused by reduced concentrations of growth hormone or IGF-I and (ii) inflammatory cytokines are produced at a time consistent with a possible role in the inhibition of milk synthesis.
在实验性大肠杆菌性乳腺炎期间，对炎性细胞因子的产生以及生长激素和胰岛素样生长因子-I（IGF-I）的浓度进行了研究，以确定它们在传染病期间动物生产性能下降中可能发挥的作用。在乳房内注入大肠杆菌后的最初10至14小时内，细菌繁殖至最高水平，达到每毫升牛奶10(4)-10(9) 菌落形成单位（cfu），且无乳腺炎的临床症状。在攻毒后约12小时开始出现快速而强烈的炎症反应，其特征为乳房肿胀、感染乳腺的牛奶中牛血清白蛋白（BSA）和体细胞计数（SCC）增加，以及直肠温度和血清皮质醇浓度升高。在24小时时，泌乳性能大幅下降，在受挑战奶牛的感染和未感染乳腺中，最大降幅分别平均为76%和63%；三头奶牛的所有乳腺暂时无乳。到6天时，所有奶牛几乎或完全清除了大肠杆菌，产奶量部分恢复。牛奶成分显示，脂肪百分比最初下降，随后上升。在大多数乳腺炎发作期间，蛋白质百分比增加，乳糖含量降低。在感染乳腺的牛奶中检测到高浓度的肿瘤坏死因子（TNF）和白细胞介素-1（IL-1），它们的出现先于或与乳腺炎症、全身反应和泌乳减少的发展同时发生。受挑战奶牛的血清生长激素浓度较高，而在乳腺炎发作期间血清IGF-I浓度变化不大。感染乳腺的乳清中IGF-I浓度从5.0 ng/ml增加到12.2 ng/ml，对侧未感染乳腺的浓度从4.4 ng/ml增加到8.5 ng/ml；感染乳腺的牛奶中IGF结合蛋白也增加。这些数据表明：（i）泌乳性能下降不是由生长激素或IGF-I浓度降低引起的；（ii）炎性细胞因子的产生时间与它们在抑制乳汁合成中可能发挥的作用一致。
