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乳房内接种大肠杆菌和金黄色葡萄球菌后乳房和乳头的早期转录事件。

Early transcriptional events in the udder and teat after intra-mammary Escherichia coli and Staphylococcus aureus challenge.

作者信息

Petzl Wolfram, Günther Juliane, Mühlbauer Katharina, Seyfert Hans-Martin, Schuberth Hans-Joachim, Hussen Jamal, Sauter-Louis Carola, Hafner-Marx Angela, Zerbe Holm

机构信息

Clinic for Ruminants with Ambulance and Herd Health Services, Centre for Clinical Veterinary Medicine, LMU Munich, Germany

Institute for Genome Biology, Leibniz Institute for Farm Animal Biology (FBN), Dummerstorf, Germany.

出版信息

Innate Immun. 2016 May;22(4):294-304. doi: 10.1177/1753425916640057. Epub 2016 Mar 24.

Abstract

Intra-mammary bacterial infections can result in harmful clinical mastitis or subclinical mastitis with persistent infections. Research during the last decades closely examined the pathophysiology of inflamed udders. Initial events after pathogen perception but before the onset of mastitis have not been examined in vivo The objective of this study was to develop a mastitis model in cows by monitoring initial transcriptional pathogen-specific host response before clinical signs occur. We applied a short-term infection model to analyse transcripts encoding chemokines, cytokines and antimicrobial molecules in the teat cistern (TC) and lobulo-alveolar parenchyma (LP) up to 3 h after challenge with E and Staphylococcus aureus Both pathogens elicited an immune reaction by 1 h after challenge. Escherichia coli induced all analysed factors (CCL20, CXCL8, TNF, IL6, IL12B, IL10, LAP, S100A9); however, S. aureus failed to induce IL12B, IL10, LAP and S100A9 expression. The E. coli-induced up-regulation was 25-105 times greater than that after S. aureus challenge. Almost all the responses were restricted to the TC. The short-term mastitis model demonstrates that a divergent pathogen-specific response is generated during the first h. It confirms that the first transcripts are generated in the TC prior to a response in the LP.

摘要

乳腺内细菌感染可导致有害的临床型乳腺炎或伴有持续性感染的亚临床型乳腺炎。过去几十年的研究对发炎乳房的病理生理学进行了仔细研究。病原体感知后但在乳腺炎发作前的初始事件尚未在体内进行研究。本研究的目的是通过监测临床症状出现前最初的病原体特异性宿主转录反应,建立奶牛乳腺炎模型。我们应用短期感染模型,分析在用大肠杆菌和金黄色葡萄球菌攻击后长达3小时的乳头池(TC)和小叶-肺泡实质(LP)中编码趋化因子、细胞因子和抗菌分子的转录本。两种病原体在攻击后1小时均引发了免疫反应。大肠杆菌诱导了所有分析的因子(CCL20、CXCL8、TNF、IL6、IL12B、IL10、LAP、S100A9);然而,金黄色葡萄球菌未能诱导IL12B、IL10、LAP和S100A9的表达。大肠杆菌诱导的上调比金黄色葡萄球菌攻击后高25至105倍。几乎所有反应都局限于乳头池。短期乳腺炎模型表明,在最初的1小时内会产生不同的病原体特异性反应。它证实了最初的转录本在小叶-肺泡实质出现反应之前在乳头池中产生。

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