title: Protective effect of CpG-DNA against mastitis induced by Staphylococcus aureus infection in a rat model.
abstract: A mastitis model in rats, induced by Staphylococcus aureus infection, was established and the protective effect of CpG-DNA on this model was determined. A S. aureus suspension containing 2 x 10(3) CFU.mL(-1) (SL group), 2 x 10(5) CFU.mL(-1) (SH group) or 100 microL PBS (CON group) was inoculated into the mammary glands of rats 72 h after parturition. The rats were euthanized at 24 h post-infection. The histopathologic changes in mammary tissue from SL were mild, whereas the structural changes of the mammary gland from SH were severe and polymorphonuclear leukocytes (PMNs) accumulated in mammary alveoli. Interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha) and N-acetyl-beta-d-Glucosaminidase (NAGase) in mammary tissue from SH were significantly increased, however, those from SL were not significantly changed. Therefore, 2 x 10(5) CFU.mL(-1) was selected to test the potential protective effect of CpG-DNA on mammary glands. CpG-DNA (200 microg) or PBS (100 microL) controls were intramuscularly injected right after parturition of rats. At 72 h post-partum, 2 x 10(5) CFU.mL(-1)of S. aureus (100 microL) were inoculated into the mammary gland of all rats and at pre-infection (0 h), 8, 16, 24, 48 and 72 h after inoculation six rats were euthanatized. CpG-DNA induced more rapid migration of PMNs from blood to mammary tissue at the initial stage of infection, stimulated the secretion of IL-6 and TNF-alpha at different time points, reduced viable S. aureus in mammary tissue and decreased the activity of NAGase. CpG-DNA also promoted the expression of its specific receptor TLR-9 mRNA in mammary tissue. In conclusion, CpG-DNA protected against S. aureus mastitis in a rat model.
authors.affiliation: Key Laboratory of Animal Physiology and Biochemistry, Ministry of Agriculture, Nanjing Agricultural University, Nanjing, PR China. zym7712@yahoo.com.cn
authors.forename: Yu-Min
authors.initials: YM
authors.lastname: Zhu
authors.forename: Jin-Feng
authors.initials: JF
authors.lastname: Miao
authors.forename: Hong-Ji
authors.initials: HJ
authors.lastname: Fan
authors.forename: Si-Xiang
authors.initials: SX
authors.lastname: Zou
authors.forename: Wei-Hua
authors.initials: WH
authors.lastname: Chen
mesh_terms: D000118:Acetylglucosaminidase / Q000097:blood / Q000378:metabolism; D000818:Animals; D018899:CpG Islands; D004247:DNA / Q000494:pharmacology*; D004195:Disease Models, Animal; D005260:Female; D015850:Interleukin-6 / Q000096:biosynthesis / Q000097:blood; D008297:Male; D008321:Mammary Glands, Animal / Q000378:metabolism / Q000473:pathology; D008413:Mastitis / Q000209:etiology / Q000517:prevention & control*; D012333:RNA, Messenger / Q000096:biosynthesis; D051381:Rats; D017207:Rats, Sprague-Dawley; D013203:Staphylococcal Infections; D013211:Staphylococcus aureus; D051217:Toll-Like Receptor 9 / Q000235:genetics; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis / Q000097:blood
chemical_list: D015850:Interleukin-6; D012333:RNA, Messenger; C489640:Tlr9 protein, rat; D051217:Toll-Like Receptor 9; D014409:Tumor Necrosis Factor-alpha; D004247:DNA; D000118:Acetylglucosaminidase