Fine D H, Goncharoff P, Schreiner H, Chang K M, Furgang D, Figurski D
Department of Oral Pathology and Biology, University of Medicine and Dentistry of New Jersey, New Jersey Dental School, Dental Research Center, 110 Bergen Street, Newark, NJ 07103, USA.
Arch Oral Biol. 2001 Nov;46(11):1065-78. doi: 10.1016/s0003-9969(01)00067-x.
Fresh isolates of Actinobacillus actinomycetemcomitans (Aa) bind avidly to surfaces in vitro, but existing in vivo studies of the adherence of Aa are limited. This study had two goals: (1) to compare the oral colonization of two isogenic strains of Aa-CU1010, a clinical isolate that expresses the adherent phenotype, and CU1012, a minimally adherent laboratory variant-and (2) to check for phenotypic reversion of these strains in a clinical setting. Rifampicin-resistant strains, developed for tracking in Sprague-Dawley rats, were tested in vitro to determine their stability and binding. In study 1, after antibiotic suppression, six rats (group I) received CU1010 in their feed. The eight rats in group II received CU1012 in their feed and four were supplemented by oral swabbing and four by gastric gavage. Group III consisted of three sham-inoculated controls. All rats were inoculated for 4 days. Microbiological data were collected at 1, 4 and 8 weeks after inoculation. Supporting data were supplied by antibody titres and clinical measures of alveolar bone loss. Study 2 consisted of six rats in each of three groups as above, but tagged strains of Aa were delivered by food alone. At all time-points in both studies, Aa was absent before inoculation and controls had no Aa or antibody to Aa. In study 1, all six rats in group I yielded positive cultures for Aa at 8 weeks. In group II, five of eight had positive cultures for Aa at 1 week, two of eight at 4 weeks and none had Aa at 8 weeks (P < or =0.001). All six rats in group I had serum anti-Aa titres compared to group II, where titres were seen in four of eight rats (P < or =0.015). In vitro data paralleled those found in vivo. No phenotypic reversion of either strain was seen in vivo. In study 2, four of six rats in group I showed Aa and had titres to Aa, while no other animals showed Aa at any time. The model provides convincing evidence that, unlike laboratory variants, clinical isolates colonize, persist and integrate into an already established, albeit reduced, econiche.
放线共生放线杆菌（Aa）的新鲜分离株在体外能强烈黏附于表面，但目前关于Aa在体内黏附情况的研究有限。本研究有两个目标：（1）比较Aa的两个同基因菌株——表达黏附表型的临床分离株CU1010和黏附性极低的实验室变异株CU1012——在口腔中的定植情况；（2）检查这些菌株在临床环境中是否发生表型逆转。为便于在斯普拉格 - 道利大鼠中追踪而构建的耐利福平菌株，在体外进行了测试以确定其稳定性和黏附性。在研究1中，在抗生素抑制后，六只大鼠（I组）在饲料中摄入CU1010。II组的八只大鼠在饲料中摄入CU1012，其中四只通过口腔擦拭补充，四只通过胃管灌洗补充。III组由三只假接种对照组成。所有大鼠接种4天。在接种后1、4和8周收集微生物学数据。通过抗体滴度和牙槽骨丧失的临床指标提供支持数据。研究2由上述三组中每组六只大鼠组成，但标记的Aa菌株仅通过食物投喂。在两项研究的所有时间点，接种前均未检测到Aa，对照组也没有Aa或抗Aa抗体。在研究1中，I组的所有六只大鼠在8周时Aa培养均呈阳性。在II组中，八只中有五只在1周时Aa培养呈阳性，八只中有两只在4周时呈阳性，八只中无一在8周时检测到Aa（P≤0.001）。I组的所有六只大鼠均有血清抗Aa滴度，而II组八只中有四只出现滴度（P≤0.015）。体外数据与体内数据相符。在体内未观察到任何一个菌株发生表型逆转。在研究2中，I组六只大鼠中有四只检测到Aa并出现抗Aa滴度，而其他动物在任何时候均未检测到Aa。该模型提供了令人信服的证据，即与实验室变异株不同，临床分离株能够定植、持续存在并整合到一个已经存在的、尽管有所减少的生态位中。
