Treponema denficola as a model for polar adhesion and cytopathogenicity of spirochetes

Ellen, Richard P.; Dawson, J R; Yang, Po Fong

doi:10.1016/0966-842x(94)90597-5

Cited by 40 publications

(38 citation statements)

References 29 publications

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“…Moreover, a chemotaxis gene cluster from T. denticola was cloned, sequenced, and analyzed (Greene and Stamm, 1999 (2001) cal, immunological, and morphological means. Possible invasion of the oral mucosa by treponemes is most likely through intracellular spaces and not through the cells themselves, as shown in vitro for oral spirochetes sharing pathogen-restricted antigens with T. pallidum (Riviere et al, 1991), and in B. burgdorferi (Ellen et al, 1994a (Weinberg and Holt, 1991;Haapasalo et al, 1992;Fenno et al, 1996). The outer sheath protein was observed in an oligomeric form (Umemoto et al, 1989;Fenno et al, 1996).…”

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confidence: 95%

“…denticola was shown to adhere to fibroblasts and epithelial cells of different origins (Weinberg and Holt, 1990;Keulers et al, 1993a,b;Ellen et al, 1994a;Haapasalo et al, 1996), as well as to extracellular matrix components present in periodontal tissues (Dawson and Ellen, 1990;Haapasalo et al, 1991) and hyaluronan (hyaluronic acid) . Recently, it was shown that oral treponemes, including T. denticola, may adhere to endothelial cells and penetrate through endothelial cell monolayers in vitro (Peters et al, 1999).…”

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Role of Treponema Denticola in Periodontal Diseases

Sela

2001

Critical Reviews in Oral Biology & Medicine

165

153

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Among periodontal anaerobic pathogens, the oral spirochetes, and especially Treponema denticola, have been associated with periodontal diseases such as early-onset periodontitis, necrotizing ulcerative gingivitis, and acute pericoronitis. Basic research as well as clinical evidence suggest that the prevalence of T. denticola, together with other proteolytic Gram-negative bacteria in high numbers in periodontal pockets, may play an important role in the progression of periodontal disease. The accumulation of these bacteria and their products in the pocket may render the surface lining periodontal cells highly susceptible to lysis and damage. T. denticola has been shown to adhere to fibroblasts and epithelial cells, as well as to extracellular matrix components present in periodontal tissues, and to produce several deleterious factors that may contribute to the virulence of the bacteria. These bacterial components include outer-sheath-associated peptidases, chymotrypsin-like and trypsin-like proteinases, hemolytic and hemagglutinating activities, adhesins that bind to matrix proteins and cells, and an outer-sheath protein with poreforming properties. The effects of T. denticola whole cells and their products on a variety of host mucosal and immunological cells has been studied extensively (Fig. 1). The clinical data regarding the presence of T. denticola in periodontal health and disease, together with the basic research results involving the role of T. denticola factors and products in relation to periodontal diseases, are reviewed and discussed in this article.

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Role of Treponema Denticola in Periodontal Diseases

Sela

2001

Critical Reviews in Oral Biology & Medicine

165

153

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“…Several potential virulence factors, including motility, are associated with these organisms (11). Compared to other spirochetes, T. denticola cells are relatively small (0.12 to 0.25 m in diameter and 6 to 16 m long) (5,46).…”

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Relationship of Treponema denticola periplasmic flagella to irregular cell morphology

et al. 1997

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Treponema denticola is an anaerobic, motile, oral spirochete associated with periodontal disease. We found that the periplasmic flagella (PFs), which are located between the outer membrane sheath and cell cylinder, influence its morphology in a unique manner. In addition, the protein composition of the PFs was found to be quite complex and similar to those of other spirochetes. Dark-field microscopy revealed that most wild-type cells had an irregular twisted morphology, with both planar and helical regions, and a minority of cells had a regular right-handed helical shape. High-voltage electron microscopy indicated that the PFs, especially in those regions of the cell which were planar, wrapped around the cell body axis in a right-handed sense. In those regions of the cell which were helical or irregular, the PFs tended to lie along the cell axis. The PFs caused the cell to form the irregular shape, as two nonmotile, PF-deficient mutants (JR1 and HL51) were no longer irregular but were right-handed helices. JR1 was isolated as a spontaneously occurring nonmotile mutant, and HL51 was isolated as a site-directed mutant in the flagellar hook gene flgE. Consistent with these results is the finding that wild-type cells with their outer membrane sheath removed were also right-handed helices similar in shape to JR1 and HL51. Purified PFs were analyzed by two-dimensional gel electrophoresis, and several protein species were identified. Western blot analysis using antisera to Treponema pallidum PF proteins along with N-terminal amino acid sequence analysis indicated T. denticola PFs are composed of one class A sheath protein of 38 kDa (FlaA) and three class B proteins of 35 kDa (FlaB1 and FlaB2) and one of 34 kDa (FlaB3). The N-terminal amino acid sequences of the FlaA and FlaB proteins of T. denticola were most similar to those of T. pallidum and Treponema phagedenis. Because these proteins were present in markedly reduced amounts or were absent in HL51, PF synthesis is likely to be regulated in a hierarchy similar to that found for flagellar synthesis in other bacteria.Spirochetes are recognized for their unique cell morphology and unusual means of motility (5, 48). In most spirochetes, the primary structural component of the cell body is a flexible yet semirigid helically shaped cell cylinder (5). Borrelia burgdorferi is an exception, since it has a rod-shaped cell cylinder (13, 15). Helical periplasmic flagella (PFs) are closely associated with the spirochetal protoplasmic cell cylinder (PC) and are embedded in the cytoplasmic membrane and cell wall near each end of the cell (5, 6, 17); each PF is inserted at only one end. Surrounding the entire cell is an outer membrane sheath (OS) (5). Genetic evidence indicates that the PFs are essential for the motility of several spirochete species (4,8,26,28,37,44). The PFs vary in number, length, and protein composition among the spirochete species. Depending on the species, the PFs may or may not overlap in the center of the cell (5, 8). PFs from most spirochete species are co...

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“…Surface-expressed and secreted proteins of T. denticola are likely to be important in its colonization and cytopathic effects (10,14,38) and in the immunological response of the host in periodontal diseases (34,35). Prominent surface antigens of between 43 and 64 kDa have been found in oral treponemes (4,14,29,30,36,39,40,42).…”

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Conservation of msp, the gene encoding the major outer membrane protein of oral Treponema spp

et al. 1997

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The major surface protein (Msp) of Treponema denticola has been implicated as a mediator of the interaction between the spirochete and the gingival epithelium in periodontal diseases. Previous studies showed that the Msp of T. denticola ATCC 35405 had porin activity, depolarized epithelial cell membranes, bound to extracellular matrix components of epithelial cells, and formed a regular hexagonal surface array in the treponemal outer membrane.

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Treponema denficola as a model for polar adhesion and cytopathogenicity of spirochetes

Cited by 40 publications

References 29 publications

Role of Treponema Denticola in Periodontal Diseases

Role of Treponema Denticola in Periodontal Diseases

Relationship of Treponema denticola periplasmic flagella to irregular cell morphology

Conservation of msp, the gene encoding the major outer membrane protein of oral Treponema spp

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