Invasive differences among <i>Porphyromonas gingivalis</i> strains from healthy and diseased periodontal sites

Jandik, K. A.; Bélanger, Myriam; Low, Sam; Dorn, Brian R.; Yang, M. C. K.; Progulske‐Fox, Ann

doi:10.1111/j.1600-0765.2007.01064.x

Cited by 24 publications

(17 citation statements)

References 59 publications

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“…As both the parental and mutant strains colonized the rat oral cavity to the same degree, these results also provide indirect evidence for the importance of intracellular invasion in P. gingivalis pathogenicity. Moreover, reduced virulence of the invasion-deficient SerB mutant corroborates reports that P. gingivalis strains isolated from diseased sites possess greater in vitro invasion efficiencies than strains isolated from healthy sites (25). Together with studies that P. gingivalis mutants lacking FimA fimbriae, a major invasion effector, are less virulent in animal models (44), a picture emerges of intracellular invasion as an important contributor to alveolar bone loss, and disruption of the invasive process renders P. gingivalis less virulent.…”

Section: Discussionsupporting

confidence: 66%

Role of Porphyromonas gingivalis Phosphoserine Phosphatase Enzyme SerB in Inflammation, Immune Response, and Induction of Alveolar Bone Resorption in Rats

Bainbridge¹,

Verma²,

Eastman³

et al. 2010

Infect Immun

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Porphyromonas gingivalis secretes a serine phosphatase enzyme, SerB, upon contact with gingival epithelial cells in vitro. The SerB protein plays a critical role in internalization and survival of the organism in epithelial cells. SerB is also responsible for the inhibition of interleukin-8 (IL-8) secretion from gingival epithelial cells infected with P. gingivalis. This study examined the ability of a P. gingivalis SerB mutant to colonize the oral cavity and induce gingival inflammation, immune responses, and alveolar bone resorption in a rat model of periodontal disease. Both P. gingivalis ATCC 33277 and an isogenic ⌬SerB mutant colonized the oral cavities of rats during the 12-week experimental period. Both of the strains induced significant (P < 0.05) systemic levels of immunoglobulin G (IgG) and isotypes IgG1, IgG2a, and IgG2b, indicating the involvement of both T helper type 1 (Th1) and Th2 responses to infection. Both strains induced significantly (P < 0.05) higher levels of alveolar bone resorption in infected rats than in sham-infected control rats. However, horizontal and interproximal alveolar bone resorption induced by the SerB mutant was significantly (P < 0.05) lower than that induced by the parental strain. Rats infected with the ⌬SerB mutant exhibited significantly higher levels of apical migration of the junctional epithelium (P < 0.01) and polymorphonuclear neutrophil (PMN) recruitment (P < 0.001) into the gingival tissues than rats infected with the wild type. In conclusion, in a rat model of periodontal disease, the SerB phosphatase of P. gingivalis is required for maximal alveolar bone resorption, and in the absence of SerB, more PMNs are recruited into the gingival tissues.

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Section: Discussionsupporting

confidence: 66%

Role of Porphyromonas gingivalis Phosphoserine Phosphatase Enzyme SerB in Inflammation, Immune Response, and Induction of Alveolar Bone Resorption in Rats

Bainbridge¹,

Verma²,

Eastman³

et al. 2010

Infect Immun

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“…It is becoming increasingly evident from this and other work that P. gingivalis represents a heterogeneous group of strains with distinct properties, in terms of proinflammatory potential, immune evasion capacity, cell invasive activity, and ability to cause disease (7, 20, 21, 30, 37). The genetic diversity of the fimA gene may, at least in part, mediate some of the virulence differences among distinct strains.…”

Section: Discussionmentioning

confidence: 99%

Differential virulence and innate immune interactions of type I and II fimbrial genotypes of Porphyromonas gingivalis

Wang

Liang

Hosur

et al. 2009

Oral Microbiology and Immunology

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Introduction The fimA-encoded fimbriae of the periodontal pathogen Porphyromonas gingivalis display genetic diversity. Type I fimbriated P. gingivalis (Pg-I) has been most widely studied at the molecular level, whereas Pg-II is the most frequent isolate from severe periodontitis. Methods To investigate virulence differences between Types I and II fimbriae, we examined strains 33277 (Pg-I) and OMZ314 (Pg-II), reciprocal swap mutants (i.e., expressing the heterologous fimbrial type), and their respective FimA-deficient derivatives. These organisms were tested in a mouse periodontitis model and in interactions with mouse macrophages, a cell type that plays important roles in chronic infections. Results Strain 33277 induced significantly more periodontal bone loss than OMZ314, and substitution of Type II fimbriae with Type I in OMZ314 resulted in a more virulent strain than the parent organism. However, the presence of Type II fimbriae was associated with increased proinflammatory and invasive activities in macrophages. Conclusion The inverse relationship between proinflammatory potential and ability to cause experimental periodontitis may suggest that an aggressive phenotype could provoke a host response that would compromise the persistence of the pathogen.

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“…Among our invasive strains, we observed different invasion efficiency rates, with serotype f strains displaying higher invasion rates than serotype e strains. Differences in invasion rates have been shown for other oral bacteria, such as P. gingivalis and S. gordonii (13,23,57), as well as for an inhabitant of the gastrointestinal flora, Streptococcus gallolyticus subsp. gallolyticus (62).…”

Section: Discussionmentioning

confidence: 99%

The Collagen-Binding Protein Cnm Is Required for Streptococcus mutans Adherence to and Intracellular Invasion of Human Coronary Artery Endothelial Cells

et al. 2011

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Streptococcus mutans is considered the primary etiologic agent of dental caries, a global health problem that affects 60 to 90% of the population, and a leading causative agent of infective endocarditis. It can be divided into four different serotypes (c, e, f, and k), with serotype c strains being the most common in the oral cavity. In this study, we demonstrate that in addition to OMZ175 and B14, three other strains (NCTC11060, LM7, and OM50E) of the less prevalent serotypes e and f are able to invade primary human coronary artery endothelial cells (HCAEC). Invasive strains were also significantly more virulent than noninvasive strains in the Galleria mellonella (greater wax worm) model of systemic disease. Interestingly, the invasive strains carried an additional gene, cnm, which was previously shown to bind to collagen and laminin in vitro. Inactivation of cnm rendered the organisms unable to invade HCAEC and attenuated their virulence in G. mellonella. Notably, the cnm knockout strains did not adhere to HCAEC as efficiently as the parental strains did, indicating that the loss of the invasion phenotype observed for the mutants was linked to an adhesion defect. Comparisons of the invasive strains and their respective cnm mutants did not support a correlation between biofilm formation and invasion. Thus, Cnm is required for S. mutans invasion of endothelial cells and possibly represents an important virulence factor of S. mutans that may contribute to cardiovascular infections and pathologies.

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Invasive differences among Porphyromonas gingivalis strains from healthy and diseased periodontal sites

Abstract: The increased invasion noted with P. gingivalis isolates from diseased sites vs. healthy sites, and the increased invasive capabilities with increasing probing depth, indicate that P. gingivalis isolates have a varying ability to invade host cells in the periodontal pocket.

Cited by 24 publications

References 59 publications

Role of Porphyromonas gingivalis Phosphoserine Phosphatase Enzyme SerB in Inflammation, Immune Response, and Induction of Alveolar Bone Resorption in Rats

Role of Porphyromonas gingivalis Phosphoserine Phosphatase Enzyme SerB in Inflammation, Immune Response, and Induction of Alveolar Bone Resorption in Rats

Differential virulence and innate immune interactions of type I and II fimbrial genotypes of Porphyromonas gingivalis

The Collagen-Binding Protein Cnm Is Required for Streptococcus mutans Adherence to and Intracellular Invasion of Human Coronary Artery Endothelial Cells

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