Chockalingam A, Paape M J, Bannerman D D
Department of Dairy and Animal Science, The Pennsylvania State University, University Park, 16802, USA.
J Dairy Sci. 2005 Jun;88(6):1986-93. doi: 10.3168/jds.S0022-0302(05)72874-5.
Among the gram-negative bacteria that cause mastitis, Escherichia coli are the most prevalent. The innate immune system provides initial protection against E. coli infection by detecting the presence of the foreign pathogens and by mounting an inflammatory response, the latter of which is mediated by cytokines such as IL-1beta, IL-8, and tumor necrosis factor (TNF)-alpha. Although changes in these cytokines during mastitis have been well-described, it is believed that other mediators moderate mammary gland inflammatory responses as well. The growth factors/cytokines transforming growth factor (TGF)-alpha, TGF-beta1, and TGF-beta2 are all expressed in the mammary gland and have been implicated in regulating mammary gland development. In other tissues, these growth factors/cytokines have been shown to moderate inflammation. The objective of the current study was to determine whether TGF-alpha, TGF-beta1, and TGF-beta2 milk concentrations were altered during the course of E. coli-induced mastitis. The contralateral quarters of 11 midlactating Holstein cows were challenged with either saline or 72 cfu of E. coli, and milk samples were collected. Basal milk levels of TGF-alpha, TGF-beta1, and TGF-beta2 were 98.81 +/- 22.69 pg/mL, 3.35 +/- 0.49 ng/mL, and 22.36 +/- 3.78 ng/mL, respectively. Analysis of whey samples derived from E. coli-infected quarters revealed an increase in milk levels of TGF-alpha within 16 h of challenge, and these increases persisted for an additional 56 h. Elevated TGF-beta1 and TGF-beta2 milk concentrations were detected in E. coli-infected quarters 32 h after challenge, and these elevations were sustained throughout the study. Because TGF-alpha, TGF-beta1, and TGF-beta2 have been implicated in mediating inflammatory processes, their induction during mastitis is consistent with a role for these molecules in mediating mammary gland host innate immune responses to infection.
在引起乳腺炎的革兰氏阴性菌中，大肠杆菌最为常见。天然免疫系统通过检测外来病原体的存在并引发炎症反应来提供对大肠杆菌感染的初始保护，后者由白细胞介素-1β、白细胞介素-8和肿瘤坏死因子-α等细胞因子介导。尽管乳腺炎期间这些细胞因子的变化已有详细描述，但人们认为其他介质也会调节乳腺的炎症反应。转化生长因子-α、转化生长因子-β1和转化生长因子-β2等生长因子/细胞因子均在乳腺中表达，并与调节乳腺发育有关。在其他组织中，这些生长因子/细胞因子已被证明可调节炎症。本研究的目的是确定在大肠杆菌诱导的乳腺炎过程中，转化生长因子-α、转化生长因子-β1和转化生长因子-β2的乳汁浓度是否发生改变。对11头处于泌乳中期的荷斯坦奶牛的对侧乳房分别用生理盐水或72 cfu的大肠杆菌进行攻击，并采集乳汁样本。转化生长因子-α、转化生长因子-β1和转化生长因子-β2的基础乳汁水平分别为98.81±22.69 pg/mL、3.35±0.49 ng/mL和22.36±3.78 ng/mL。对来自大肠杆菌感染乳房的乳清样本分析显示，攻击后16小时内乳汁中转化生长因子-α水平升高，且这些升高持续了另外56小时。攻击后32小时在大肠杆菌感染的乳房中检测到转化生长因子-β1和转化生长因子-β2的乳汁浓度升高，且这些升高在整个研究过程中持续存在。由于转化生长因子-α、转化生长因子-β1和转化生长因子-β2与介导炎症过程有关，它们在乳腺炎期间的诱导与这些分子在介导乳腺宿主对感染的天然免疫反应中的作用一致。
