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A Listeria monocytogenes ST2 clone lacking chitinase ChiB from an outbreak of non-invasive gastroenteritis

机译:非侵袭性胃肠炎暴发时缺乏几丁质酶ChiB的李斯特菌李斯特菌ST2克隆

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An outbreak with a remarkable Listeria monocytogenes clone causing 163 cases of non-invasive listeriosis occurred in Germany in 2015. Core genome multi locus sequence typing grouped non-invasive outbreak isolates and isolates obtained from related food samples into a single cluster, but clearly separated genetically close isolates obtained from invasive listeriosis cases. A comparative genomic approach identified a premature stop codon in the chiB gene, encoding one of the two L. monocytogenes chitinases, which clustered with disease outcome. Correction of this premature stop codon in one representative gastroenteritis outbreak isolate restored chitinase production, but effects in infection experiments were not found. While the exact role of chitinases in virulence of L. monocytogenes is still not fully understood, our results now clearly show that ChiB-derived activity is not required to establish L. monocytogenes gastroenteritis in humans. This limits a possible role of ChiB in human listeriosis to later steps of the infection.
机译:2015年,德国爆发了具有明显单核细胞增生性李斯特菌克隆的暴发,导致163例非侵入性李斯特菌病。核心基因组多基因座序列分型将非侵入性暴发分离株和从相关食物样品中获得的分离株分组为一个簇,但在基因上明显分开从侵袭性李斯特菌病病例中获得的分离株。比较基因组学方法在chiB基因中鉴定了一个过早的终止密码子,该密码子编码两个单核细胞增生李斯特菌几丁质酶之一,并与疾病结局成簇。在一个代表性的肠胃炎爆发分离物中纠正这种过早的终止密码子恢复了几丁质酶的产生,但未发现对感染实验的影响。尽管几丁质酶在单核细胞增生李斯特氏菌毒力中的确切作用仍未完全了解,但我们的结果现在清楚地表明,在人中建立单核细胞增生李斯特氏菌肠胃炎不需要ChiB衍生的活性。这将ChiB在人类李斯特菌病中的可能作用限制到感染的后续步骤。

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