中文摘要：

[目的]建立金黄色葡萄球菌（Staphylococcus aureus）感染的大鼠乳腺炎模型,并观察CpG-DNA对乳腺的保护作用.[方法]18只雌鼠分3组（n=6）,产后72h分别灌注磷酸盐缓冲液（phosphate buffer solution,PBS）（C组）、2×10^5CFU·ml^-1（L组）和2×10^12CFU·ml^-1 （H组）金葡菌到第四对乳腺内,24 h处死.L组乳腺病变轻微,H组腺泡结构破坏严重,并有大量嗜中性粒细胞（polymorphonuclear neutrophils,PMN）浸润;H组乳腺组织TNF-α、IL-6水平显著上升.选择2×10^12CFU·ml^-1为诱发剂量观察CpG-DNA对乳腺的保护作用：72只雌鼠分成对照和试验组（n=36）,对照组产后0 h肌注PBS;试验组肌注CpG-DNA,72 h后灌注金葡菌到第四对乳腺内.分别于灌注前（定义为0 h）,灌注后8、16、24、48和72 h（n=6）处死.[结果]感染初期试验组乳腺腺泡内PMN较对照组浸润迅速.试验组乳腺组织白细胞介素-6（interleukine-6,IL-6）在16、24和48 h显著高于对照组.CpG-DNA能显著提高0、24和72 h乳腺组织肿瘤坏死因子-α（tumor necrosis factor-α,TNF-α）水平.试验组8、16和72 h的乳腺组织金葡菌数显著低于对照组.CpG-DNA能显著提高乳腺组织中其特异性受体TLR-9（toll-like receptor-9）mRNA表达水平.[结论]CpG-DNA对金葡菌感染诱发大鼠乳腺炎的乳腺有保护作用.

英文摘要：

[ Objective ] The study aimed to establish a rat mastitis model induced by a Staphylococcus aureus infection and to observe the protective effect of CpG-DNA on mammary glands of rats with mastitis. [Method] 18 rats were divided into 3 groups. 2×10^5CFU·ml^-1（L group）, 2×10^12CFU·ml^-1 of S. aureus （H group） and phosphate-buffered saline （C group） were inoculated into the mammary glands 72 h after parturition. All the rats were sacrificed at 24 h after infection. The pathological variance of mammary gland from L was mild, but the mammary gland structure from H was seriously destructed, as polymorphonuclear neutrophils （PMN） were accumulated in alveoli. TNF-α and IL-6 in mammary gland from H elevated significantly. So the 2×10^12CFU·ml^-1 was chosen to evaluate the effect of CpG-DNA on mammary gland. 72 rats were divided into control and treatment group. PBS（control） and CpG-DNA（treatment ） were injected intramuscularly into rats after parturition. Then 2×10^12CFU·ml^-1 of S. aureus were inoculated into the fourth mammary glands 72 h after parturition. Before （defined as Oh） and after 8, 16, 24, 48 and 72 h （n=6） of inoculation, all the rats were sacrificed. [Result] The PMN infiltrated to the mammary gland more promptly in treatment group than control at the initial stage of infection. IL-6 in mammary gland from treatment group was significant higher than the control at 16, 24 and 48 h. CpG-DNA could elicit significant elevated TNF-α in mammary gland before infection, 24 and 72 h after infection, Viable S. aureus counts in treatment group were significantly lower at 8,16 and 72 h postinfection than control. CpG-DNA induced higher level of its specific receptor TLR-9 mRNA in mammary gland than control. [Conlusion] CpG-DNA protected the mammary gland against mastitis by S. aureus infection in rat.