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首页> 外文期刊>Clinical and diagnostic laboratory immunology >Mastitis Increases Mammary mRNA Abundance of β-Defensin 5, Toll-Like-Receptor 2 (TLR2), and TLR4 but Not TLR9 in Cattle
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Mastitis Increases Mammary mRNA Abundance of β-Defensin 5, Toll-Like-Receptor 2 (TLR2), and TLR4 but Not TLR9 in Cattle

机译：乳腺炎增加牛的β-防御素5，Toll样受体2（TLR2）和TLR4而不是TLR9的乳腺mRNA丰度

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Coordination of the primary defense mechanisms against pathogens relies on the appropriate expression of pathogen recognition receptors (PRRs) triggering the early release of effector molecules of the innate immune system. To analyze the impact of this system on the counteraction of infections of the mammary gland (mastitis), we characterized the bovine gene encoding the key PRR Toll-like receptor 9 (TLR9) and mapped its precise position on chromosome BTA22. The sequence information was used to establish real-time PCR quantification assays to measure the mRNA abundances of TLR9, TLR2, and TLR4 together with those of β-defensin 5 (BNBD5), an early bactericidal effector molecule of the innate system, in healthy and infected mammary glands. Mastitis strongly increased (4- to 13-fold) the mRNA abundances of all of these genes except TLR9. Slight subclinical infections already caused a substantial increase in the copy numbers, though they did so the least for TLR9. Induction was not systemic, since mRNA abundance was low in uninfected control quarters of the udder but high in the severely infected quarters of the same animal. The number of TLR2 copies correlated well with those of TLR4, indicating coordinated regulation of these two PRRs during infection of the udder. Their coordinated regulation explains our unexpected observation that pure Staphylococcus aureus infections caused a strong increase also in TLR4 mRNA abundance. In situ hybridizations revealed that BNBD5 is expressed predominantly in the mammary epithelial cells (MEC) of the infected gland. Our data therefore suggest a significant contribution of the innate immune system to counteract mastitis and attribute a prominent effector function to the MEC.
机译：对抗病原体的主要防御机制的协调取决于病原体识别受体（PRR）的适当表达，从而触发先天免疫系统效应分子的早期释放。为了分析该系统对乳腺（乳腺炎）感染抵抗作用的影响，我们表征了编码关键PRR Toll样受体9（TLR9）的牛基因，并将其精确定位在BTA22染色体上。序列信息用于建立实时PCR定量测定法，以测量健康和正常环境中TLR9，TLR2和TLR4以及先天系统的早期杀菌效应分子β-防御素5（BNBD5）的mRNA丰度。被感染的乳腺。乳腺炎使所有这些基因（TLR9除外）的mRNA丰度大大增加（4到13倍）。轻微的亚临床感染已经导致了拷贝数的大幅增加，尽管对于TLR9而言，拷贝数却最少。诱导不是全身性的，因为在未感染的乳腺对照区中，mRNA丰度较低，而在同一只动物的严重感染区中，mRNA丰度较高。 TLR2拷贝数与TLR4拷贝数相关性很好，表明在乳房感染期间这两个PRR的协调调节。他们的协调调节解释了我们出乎意料的观察结果，即纯金黄色葡萄球菌感染也导致TLR4 mRNA丰度也大大增加。原位杂交表明，BNBD5主要在感染腺的乳腺上皮细胞（MEC）中表达。因此，我们的数据表明先天免疫系统对抵抗乳腺炎和将显着的效应子功能归因于MEC具有重要作用。

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