Escherichia coli, but not Staphylococcus aureus triggers an early increased expression of factors contributing to the innate immune defense in the udder of the cow
Escherichia coli, but not Staphylococcus aureus triggers an early increased expression of factors contributing to the innate immune defense in the udder of the cow
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DOI：
10.1051/vetres:2007057
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发表时间：
2008-03-01
影响因子：
4.4
通讯作者：
Schuberth, Hans-Joachim
中科院分区：
文献类型：
--
作者：
Petzl, Wolfram;Zerbe, Holm;Schuberth, Hans-Joachim
乳房感染的结果受病原体种类的影响。我们建立了一个严格定义的感染模型，以更好地分析这些病原体特异性影响的未知分子原因，使用大肠杆菌和金黄色葡萄球菌菌株先前从乳腺炎的现场病例中分离出来。用500 CFU E.大肠杆菌（n = 4）在剔除前6 h、12 h和24 h进行。攻毒后12 h，所有动物均出现急性临床型乳腺炎体征：体细胞计数（SCC）增加、产奶量降低、白细胞减少、发热和乳房肿胀。接种10 000 CFU S.金黄色葡萄球菌培养24小时（n = 4）没有显示或仅显示出适度的乳腺炎临床体征。然而，S.金黄色葡萄球菌在接种72 h - 84 h的动物中引起临床症状。实时荧光定量PCR结果表明，E.大肠杆菌接种强烈和显着上调β-防御素，TLR 2和TLR 4在病原体接种的乳房季度以及在乳房淋巴结的表达。TLR 3和TLR 6不受感染的显著调节。免疫组织化学鉴定乳腺上皮细胞为上调TLR 2和β-防御素表达的位点。S.相反，在病原体接种后的前24小时内，金黄色葡萄球菌没有显著调节这些基因中任何一个的表达。仅在接种后84小时，在六个病原体接种的区中的五个中，β-防御素的表达而非TLR的表达显著上调（> 20倍）。使用所建立的乳腺炎模型，数据清楚地表明诱导的病原体受体和防御分子的时间动力学的病原体依赖性差异。
The outcome of an udder infection is influenced by the pathogen species. We established a strictly defined infection model to better analyze the unknown molecular causes for these pathogen-specific effects, using Escherichia coli and Staphylococcus aureus strains previously asseverated from field cases of mastitis. Inoculation of quarters with 500 CFU of E. coli ( n = 4) was performed 6 h, 12 h, and 24 h before culling. All animals showed signs of acute clinical mastitis 12 h after challenge: increased somatic cell count (SCC), decreased milk yield, leukopenia, fever, and udder swelling. Animals inoculated with 10 000 CFU of S. aureus for 24 h ( n = 4) showed no or only modest clinical signs of mastitis. However, S. aureus caused clinical signs in animals, inoculated for 72 h - 84 h. Real-time PCR proved that E. coli inoculation strongly and significantly upregulated the expression of beta-defensins, TLR2 and TLR4 in the pathogen inoculated udder quarters as well as in mammary lymph nodes. TLR3 and TLR6 were not significantly regulated by the infections. Immuno-histochemistry identified mammary epithelial cells as sites for the upregulated TLR2 and beta-defensin expression. S. aureus, in contrast, did not significantly regulate the expression of any of these genes during the first 24 h after pathogen inoculation. Only 84 h after inoculation, the expression of beta-defensins, but not of TLRs was significantly (> 20 fold) upregulated in five out of six pathogen inoculated quarters. Using the established mastitis model, the data clearly demonstrate a pathogen-dependent difference in the time kinetics of induced pathogen receptors and defense molecules.