Colonization and Persistence of Labeled and "Foreign" Strains of Aggregatibacter actinomycetemcomitans Inoculated into the Mouths of Rhesus Monkeys.
Colonization and Persistence of Labeled and "Foreign" Strains of Aggregatibacter actinomycetemcomitans Inoculated into the Mouths of Rhesus Monkeys.
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DOI：
10.13188/2377-987x.1000005
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发表时间：
2015-01-01
期刊：
影响因子：
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通讯作者：
Godboley, Dipti
中科院分区：
文献类型：
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作者：
Fine, Daniel H;Karched, Maribasappa;Godboley, Dipti
放线菌聚集菌 (Aa) 是一种病原体，是可导致人类牙周炎的细菌群落的一部分。我们的目的是开发一种将标记的 Aa 口服接种到合适宿主的模型，以研究增强或抑制其持久性的 Aa 特性和生态因素。对灵长类动物进行 Aa 筛选，以选择定植研究的宿主。选择猕猴（恒河猴/Rh）。分离出 Rh Aa 菌株，进行测序和功能分析，以便与人类菌株进行比较。评估了接种前微生物净化的“最佳”方法。研究了三组；第1组（N=5）接种Aa大观霉素抗性（SpecR）Rh菌株4.35，第2组（N=5）接种Aa SpecR人菌株IDH 781，第3组（N=5）接种未接种的对照。高剂量口服接种后，重复喂食掺有 SpecRAa 的煎饼。将接种后 1、2、3 和 4 周基线时收集的脸颊、舌头和菌斑样本涂在琼脂上； 1) 对 Aa 有选择性，2) 富集总计数，3) 含有 50 g/ml Spec。通过菌落形态学和 DNA 分析来鉴定 Aa。 Rh 和人类 Aa 的基因组同一性 > 93-98%。在体外，Rh Aa 比 IDH 781 更好地附着在组织上 (p < 0.05)。 SpecR IDH 781 在任何时间均未从任何组织中回收；而在所有猴子中，RhSpecR 4.35 始终在斑块中检测到，但从未在舌头或脸颊中检测到（> 1 * 105 菌落/ml；p < 0.001）。总之，灵长类动物模型为研究 Aa 菌株整合到减少但已建立的口腔栖息地提供了一个有用的平台。在所有收集期间，在菌斑中始终检测到源自灵长类动物的 SpecRAa；然而，从未检测到人源 Aa。该模型展示了微生物和组织特异性。
Aggregatibacter actinomycetemcomitans (Aa) is a pathobiont and part of a consortium of bacteria that can lead to periodontitis in humans. Our aim was to develop a model for oral inoculation of labeled Aa into a suitable host in order to study Aa traits and ecological factors that either enhance or repress its persistence. Primate species were screened for Aa to select a host for colonization studies. Macaca mulatta (Rhesus/Rh) was selected. Rh Aa strains were isolated, subjected to sequencing and functional analysis for comparison to human strains. "Best" methods for microbial decontamination prior to inoculation were assessed. Three groups were studied; Group 1 (N=5) was inoculated with Aa Spectinomycin resistant (SpecR) Rh strain 4.35, Group 2 (N=5) inoculated with Aa SpecR human strain IDH 781, and Group 3 (N=5) the un-inoculated control. Repeated feeding with pancakes spiked with SpecRAa followed high dose oral inoculation. Cheek, tongue, and plaque samples collected at baseline 1, 2, 3, and 4 weeks after inoculation were plated on agar; 1) selective for Aa, 2) enriched for total counts, and 3) containing 50 g/ml of Spec. Aa was identified by colonial morphology and DNA analysis. Rh and human Aa had > 93-98 % genome identity. Rh Aa attached to tissues better than IDH 781 in vitro (p < 0.05). SpecR IDH 781 was not recovered from any tissue at any time; whereas, RhSpecR 4.35 was detected in plaque, but never tongue or cheek, in all monkeys at all times (> 1 * 105 colonies/ml; p < 0.001). In conclusion, the primate model provides a useful platform for studying integration of Aa strains into a reduced but established oral habitat. Primate derived SpecRAa was consistently detected in plaque at all collection periods; however, human derived Aa was never detected. The model demonstrated both microbial as well as tissue specificity.