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Glycan cross-feeding supports mutualism between Fusobacterium and the vaginal microbiota.
PLOS Biology ( IF 7.8 ) Pub Date : 2020-08-25 , DOI: 10.1371/journal.pbio.3000788
Kavita Agarwal 1, 2 , Lloyd S Robinson 1, 2 , Somya Aggarwal 1, 2 , Lynne R Foster 1, 2 , Ariel Hernandez-Leyva 2, 3 , Hueylie Lin 1, 2 , Brett A Tortelli 2, 4 , Valerie P O'Brien 1, 2 , Liza Miller 1, 2 , Andrew L Kau 2, 3 , Hilary Reno 5 , Nicole M Gilbert 2, 6, 7 , Warren G Lewis 1, 2 , Amanda L Lewis 1, 2, 6
Affiliation  

Women with bacterial vaginosis (BV), an imbalance of the vaginal microbiome, are more likely to be colonized by potential pathogens such as Fusobacterium nucleatum, a bacterium linked with intrauterine infection and preterm birth. However, the conditions and mechanisms supporting pathogen colonization during vaginal dysbiosis remain obscure. We demonstrate that sialidase activity, a diagnostic feature of BV, promoted F. nucleatum foraging and growth on mammalian sialoglycans, a nutrient resource that was otherwise inaccessible because of the lack of endogenous F. nucleatum sialidase. In mice with sialidase-producing vaginal microbiotas, mutant F. nucleatum unable to consume sialic acids was impaired in vaginal colonization. These experiments in mice also led to the discovery that F. nucleatum may also “give back” to the community by reinforcing sialidase activity, a biochemical feature of human dysbiosis. Using human vaginal bacterial communities, we show that F. nucleatum supported robust outgrowth of Gardnerella vaginalis, a major sialidase producer and one of the most abundant organisms in BV. These results illustrate that mutually beneficial relationships between vaginal bacteria support pathogen colonization and may help maintain features of dysbiosis. These findings challenge the simplistic dogma that the mere absence of “healthy” lactobacilli is the sole mechanism that creates a permissive environment for pathogens during vaginal dysbiosis. Given the ubiquity of F. nucleatum in the human mouth, these studies also suggest a possible mechanism underlying links between vaginal dysbiosis and oral sex.



中文翻译:

聚糖交叉喂食支持镰刀菌和阴道微生物群之间的相互关系。

细菌性阴道病(BV)(阴道微生物组失衡)的女性更有可能被潜在的病原体定殖,例如与子宫内感染和早产有关的细菌Fusobacterium nucleatum。然而,在阴道失调期间支持病原体定殖的条件和机制仍然不清楚。我们表明,唾液酸酶的活性,BV的诊断功能,促进˚F。哺乳动物唾液聚糖上的细胞核觅食和生长,由于缺乏内源性F,否则无法获得这种营养资源。唾液酸酶。在用唾液酸酶生产阴道microbiotas,突变小鼠˚F无法消耗唾液酸在阴道定植中受损。这些在老鼠身上的实验也导致了F的发现。核仁还可以通过增强唾液酸酶活性(人类营养不良的生化特征)来“回馈”社区。使用人阴道的细菌群落,我们表明,˚F支持阴道加德纳菌的健壮生长是唾液酸酶的主要生产商,也是BV中含量最高的生物之一。这些结果表明,阴道细菌之间的互利关系支持病原体定殖,并可能有助于维持营养不良的特征。这些发现挑战了简单化的教条,即仅缺乏“健康”乳杆菌是在阴道营养不良期间为病原体创造宽松环境的唯一机制。鉴于F的普遍存在。这些研究还表明,在人类口腔中的中存在潜在的机制,这是阴道营养不良与口交之间潜在联系的潜在机制。

更新日期:2020-08-26
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