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首页> 外文期刊>Infection and immunity >Genome-Wide Mapping of Cystitis Due to Streptococcus agalactiae and Escherichia coli in Mice Identifies a Unique Bladder Transcriptome That Signifies Pathogen-Specific Antimicrobial Defense against Urinary Tract Infection
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Genome-Wide Mapping of Cystitis Due to Streptococcus agalactiae and Escherichia coli in Mice Identifies a Unique Bladder Transcriptome That Signifies Pathogen-Specific Antimicrobial Defense against Urinary Tract Infection

机译：小鼠无乳链球菌和大肠杆菌引起的膀胱炎的基因组全图确定了一个独特的膀胱转录组，该转录组表示针对尿路感染的病原体特异性抗菌素防御。

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The most common causes of urinary tract infections (UTIs) are Gram-negative pathogens such as Escherichia coli; however, Gram-positive organisms, including Streptococcus agalactiae, or group B streptococcus (GBS), also cause UTI. In GBS infection, UTI progresses to cystitis once the bacteria colonize the bladder, but the host responses triggered in the bladder immediately following infection are largely unknown. Here, we used genome-wide expression profiling to map the bladder transcriptome of GBS UTI in mice infected transurethrally with uropathogenic GBS that was cultured from a 35-year-old women with cystitis. RNA from bladders was applied to Affymetrix Gene-1.0ST microarrays; quantitative reverse transcriptase PCR (qRT-PCR) was used to analyze selected gene responses identified in array data sets. A surprisingly small significant-gene list of 172 genes was identified at 24 h; this compared to 2,507 genes identified in a side-by-side comparison with uropathogenic E. coli (UPEC). No genes exhibited significantly altered expression at 2 h in GBS-infected mice according to arrays despite high bladder bacterial loads at this early time point. The absence of a marked early host response to GBS juxtaposed with broad-based bladder responses activated by UPEC at 2 h. Bioinformatics analyses, including integrative system-level network mapping, revealed multiple activated biological pathways in the GBS bladder transcriptome that regulate leukocyte activation, inflammation, apoptosis, and cytokine-chemokine biosynthesis. These findings define a novel, minimalistic type of bladder host response triggered by GBS UTI, which comprises collective antimicrobial pathways that differ dramatically from those activated by UPEC. Overall, this study emphasizes the unique nature of bladder immune activation mechanisms triggered by distinct uropathogens.
机译：尿路感染（UTI）的最常见原因是革兰氏阴性病原体，例如大肠杆菌。但是，包括无乳链球菌或B组链球菌（GBS）在内的革兰氏阳性生物也会引起UTI。在GBS感染中，一旦细菌定植在膀胱中，UTI就会发展为膀胱炎，但是感染后立即在膀胱中触发的宿主反应在很大程度上是未知的。在这里，我们使用了全基因组表达谱来绘制尿道致病性GBS的经尿道感染的小鼠中GBS UTI的膀胱转录组图谱，该小鼠是由35岁的膀胱炎女性培养而成的。将来自膀胱的RNA应用于Affymetrix Gene-1.0ST微阵列;定量逆转录酶PCR（qRT-PCR）用于分析在阵列数据集中鉴定的选定基因反应。在24小时内发现了172个基因的惊人小显着基因列表;与尿路致病性大肠杆菌（UPEC）并排比较时发现的2,507个基因相比。尽管在这个早期的时间点，膀胱细菌载量很高，但根据阵列，在GBS感染的小鼠中，没有基因在2 h时表达显着改变。在2 h时，没有明显的早期宿主对GBS的反应与UPEC激活的基础广泛的膀胱反应并存。生物信息学分析，包括集成的系统级网络映射，揭示了GBS膀胱转录组中多个激活的生物途径，这些途径调节白细胞激活，炎症，凋亡和细胞因子趋化因子的生物合成。这些发现定义了一种由GBS UTI触发的新颖，简约的膀胱宿主反应类型，其中包括与UPEC激活的途径明显不同的集体抗菌途径。总的来说，这项研究强调了由独特的尿路致病菌触发的膀胱免疫激活机制的独特性质。

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