Vangroenweghe F, Lamote I, Burvenich C
Milk Secretion and Mastitis Research Center, Department of Physiology-Biochemistry-Biometrics, Faculty of Veterinary Medicine, Ghent University, Salisburylaan 133, 9820 Merelbeke, Belgium.
Domest Anim Endocrinol. 2005 Aug;29(2):283-93. doi: 10.1016/j.domaniend.2005.02.016. Epub 2005 Mar 11.
Incidence of clinical mastitis is highest at drying off and during the periparturient period. Intramammary Escherichia coli infection in high-yielding cows can show a severe clinical response during the early post-partum period. Severe clinical mastitis is mainly determined by cow factors, in particular the functionality of the circulating polymorphonuclear leukocytes (PMN) which are recruited to the mammary gland during the inflammatory reaction. There is a co-incidence between the periods of highest incidence of clinical mastitis and specific structural changes in the mammary gland. During the periparturient period, marked changes in various systemic and local hormones are related to the secretory state of the mammary gland epithelium (lactogenesis). Estrogen and progesterone induce proliferation of the mammary epithelium throughout gestation and act as survival factors in different tissues, although conflicting data have been reported on their effect on PMN oxidative burst. Somatotropin (STH), responsible for maintenance of lactation in ruminants, has been shown to positively influence innate immunity and a more rapid recovery in milk production of severely affected animals. The concentration of STH, and as a result also IGF-I levels is, however, quite low during early lactation. IGF-I and its regulating binding proteins are associated with cell survival, modulation of apoptosis and functionality of PMN in humans. During early lactation, bio-availability of IGF-I is decreased, which might reduce its stimulating effects on PMN quality and functionality. PRL, concomitantly known as a lactogenic hormone and an immunoregulatory cytokine, has also been associated with modulation of the immune system. It is expected that in periparturient animals, hormone changes could interfere with the immune response and the clinical response of mastitis.
临床型乳腺炎的发病率在干奶期和围产期最高。高产奶牛的乳房内大肠杆菌感染在产后早期可能会表现出严重的临床反应。严重的临床型乳腺炎主要由奶牛因素决定，特别是循环多形核白细胞（PMN）的功能，这些细胞在炎症反应期间被募集到乳腺。临床型乳腺炎发病率最高的时期与乳腺的特定结构变化同时出现。在围产期，各种全身和局部激素的显著变化与乳腺上皮的分泌状态（泌乳生成）有关。雌激素和孕酮在整个妊娠期诱导乳腺上皮细胞增殖，并在不同组织中作为存活因子起作用，尽管关于它们对PMN氧化爆发的影响存在相互矛盾的数据。生长激素（STH）负责反刍动物的泌乳维持，已被证明对先天免疫有积极影响，并能使严重受影响动物的产奶量更快恢复。然而，在泌乳早期，STH的浓度以及因此IGF-I的水平相当低。IGF-I及其调节结合蛋白与人类细胞存活、细胞凋亡调节和PMN功能有关。在泌乳早期，IGF-I的生物利用度降低这可能会降低其对PMN质量和功能的刺激作用。催乳素（PRL），同时被称为泌乳激素和免疫调节细胞因子，也与免疫系统的调节有关。预计在围产期动物中，激素变化可能会干扰乳腺炎的免疫反应和临床反应。
