Kolenbrander P E, Parrish K D, Andersen R N, Greenberg E P
Laboratory of Microbial Ecology, National Institute of Dental Research, Bethesda, Maryland 20892-4350, USA.
Infect Immun. 1995 Dec;63(12):4584-8. doi: 10.1128/iai.63.12.4584-4588.1995.
A total of 22 strains of Treponema spp. including members of all four named human oral species were tested for coaggregation with 7 strains of oral fusobacteria, 2 strains of nonoral fusobacteria, and 45 strains of other oral bacteria, which included actinobacilli, actinomyces, capnocytophagae, eubacteria, porphyromonads, prevotellae, selenomonads, streptococci, and veillonellae. None of the treponemes coaggregated with any of the latter 45 oral strains or with the two nonoral fusobacteria. All treponemes, eight Treponema denticola strains, eight T. socranskii strains, four oral pectinolytic treponemes, one T. pectinovorum strain, and one T. vincentii strain coaggregated with at least one strain of the fusobacteria tested as partners. The partners consisted of one strain of Fusobacterium periodonticum, five F. nucleatum strains including all four subspecies of F. nucleatum, and a strain of F. simiae obtained from the dental plaque of a monkey. In the more than 100 coaggregations observed, the fusobacterial partner was heat inactivated (85 degrees C for 30 min), while the treponemes were unaffected by the heat treatment. Furthermore, the fusobacteria were usually inactivated by proteinase K treatment, and the treponemes were not affected. Only the T. denticola coaggregations were inhibited by lactose and D-galactosamine. None were inhibited by any of 23 other different sugars or L-arginine. Intragenic coaggregations were seen among the subspecies of F. nucleatum and with F. periodonticum, and none were inhibited by any of the sugars tested or by L-arginine. No intrageneric coaggregations were observed among the treponemes. These data indicate that the human oral treponemes show a specificity for oral fusobacteria as coaggregation partners. Such cell-to cell contact may facilitate efficient metabolic communication and enhance the proliferation of each cell in the progressively more severe stages of periodontal disease.
共对22株密螺旋体属菌株进行了检测，其中包括所有四种已命名的人类口腔菌种的成员，检测它们与7株口腔梭杆菌、2株非口腔梭杆菌以及45株其他口腔细菌的共聚情况，其他口腔细菌包括放线杆菌、放线菌、二氧化碳嗜纤维菌、真细菌、卟啉单胞菌、普雷沃菌、硒单胞菌、链球菌和韦荣球菌。没有一种密螺旋体与后45种口腔菌株或两种非口腔梭杆菌发生共聚。所有密螺旋体，8株具核梭杆菌菌株、8株索氏密螺旋体菌株、4株口腔果胶分解密螺旋体、1株果胶密螺旋体菌株和1株文森特密螺旋体菌株，都与至少一种作为伙伴进行检测的梭杆菌菌株发生了共聚。这些伙伴包括1株牙周梭杆菌、5株具核梭杆菌菌株（包括具核梭杆菌的所有四个亚种）以及从一只猴子的牙菌斑中分离得到的1株猕猴梭杆菌。在观察到的100多次共聚中，梭杆菌伙伴经热灭活（85摄氏度处理30分钟），而密螺旋体不受热处理的影响。此外，梭杆菌通常会被蛋白酶K处理灭活，而密螺旋体不受影响。只有具核梭杆菌的共聚受到乳糖和D - 半乳糖胺的抑制。23种其他不同的糖或L - 精氨酸均未对其产生抑制作用。在具核梭杆菌的亚种之间以及与牙周梭杆菌之间观察到了种内共聚，并且任何测试的糖或L - 精氨酸均未对其产生抑制作用。在密螺旋体之间未观察到属内共聚。这些数据表明，人类口腔密螺旋体对口腔梭杆菌作为共聚伙伴具有特异性。这种细胞间接触可能有助于有效的代谢通讯，并在牙周病逐渐加重的阶段促进每个细胞的增殖。
