scholarly journals Immune Response and Alveolar Bone Resorption in a Mouse Model of Treponema denticola Infection

2008 ◽  
Vol 77 (2) ◽  
pp. 694-698 ◽  
Author(s):  
Song F. Lee ◽  
Elisoa Andrian ◽  
Elden Rowland ◽  
Ignacio Christian Marquez
Keyword(s):  
Immune Response ◽  
Bone Resorption ◽  
Alveolar Bone ◽  
Interleukin 10 ◽  
Oral Infection ◽  
Infection Model ◽  
Treponema Denticola ◽  
Outer Sheath ◽  
Oral Inoculation ◽  
Animal Infection

ABSTRACT Treponema denticola is considered to be an agent strongly associated with periodontal disease. The lack of an animal infection model has hampered the understanding of T. denticola pathogenesis and the host's immune response to infection. In this study, we have established an oral infection model in mice, demonstrating that infection by oral inoculation is feasible. The presence of T. denticola in the oral cavities of the animals was confirmed by PCR. Mice given T. denticola developed a specific immune response to the bacterium. The antibodies generated from the infection were mainly of the immunoglobulin G1 subclass, indicating a Th2-tilted response. The antibodies recognized 11 T. denticola proteins, of which a 62-kDa and a 53-kDa protein were deemed immunodominant. The two proteins were identified, respectively, as dentilisin and the major outer sheath protein by mass spectrometry. Splenocytes cultured from the infected mice no longer produced interleukin-10 and produced markedly reduced levels of gamma interferon relative to those produced by naïve splenocytes upon stimulation with T. denticola. Mandibles of infected mice showed significantly greater bone resorption (P < 0.01) than those of mock-infected controls.

γδ T Cells Differentially Regulate Bone Loss in Periodontitis Models

2021 ◽  
pp. 002203452110428
Author(s):  
O. Barel ◽  
Y. Aizenbud ◽  
Y. Tabib ◽  
Y. Jaber ◽  
A. Leibovich ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Bone Loss ◽  
Immune Responses ◽  
Alveolar Bone ◽  
Γδ T Cells ◽  
Oral Infection ◽  
Alveolar Bone Loss ◽  
Infection Model ◽  
The Impact

γδ T cells are nonclassical T lymphocytes representing the major T-cell population at epithelial barriers. In the gingiva, γδ T cells are enriched in epithelial regions adjacent to the biofilm and are considered to regulate local immunity to maintain host-biofilm homeostatic interactions. This delicate balance is often disrupted resulting in the development of periodontitis. Previous studies in mice lacking γδ T cells from birth ( Tcrd-/- mice) examined the impact of these cells on ligature-induced periodontitis. Data obtained from those studies proposed either a protective effect or no impact to γδ T cells in this setting. Here, we addressed the role of γδ T cells in periodontitis using the recently developed Tcrd-GDL mice, enabling temporal ablation of γδ T cells. Specifically, the impact of γδ T cells during periodontitis was examined in 2 modalities: the ligature model and the oral infection model in which the pathogen Porphyromonas gingivalis was administrated via successive oral gavages. Ablation of γδ T cells during ligature-induced periodontitis had no impact on innate immune cell recruitment to the ligated gingiva. In addition, the number of osteoclasts and subsequent alveolar bone loss were unaffected. However, γδ T cells play a pathologic role during P. gingivalis infection, and their absence prevented alveolar bone loss. Further analysis revealed that γδ T cells were responsible for the recruitment of neutrophils and monocytes to the gingiva following the exposure to P. gingivalis. γδ T-cell ablation also downregulated osteoclastogenesis and dysregulated long-term immune responses in the gingiva. Collectively, this study demonstrates that whereas γδ T cells are dispensable to periodontitis induced by the ligature model, they play a deleterious role in the oral infection model by facilitating pathogen-induced bone-destructive immune responses. On a broader aspect, this study highlights the complex immunopathologic mechanisms involved in periodontal bone loss.

scholarly journals Prevalence of Local Immune Response against Oral Infection in a Drosophila/Pseudomonas Infection Model

2006 ◽  
Vol 2 (6) ◽  
pp. e56 ◽  
Author(s):  
Peter Liehl ◽  
Mark Blight ◽  
Nicolas Vodovar ◽  
Frédéric Boccard ◽  
Bruno Lemaitre
Keyword(s):  
Immune Response ◽  
Oral Infection ◽  
Infection Model ◽  
Local Immune Response ◽  
Pseudomonas Infection

scholarly journals Adhesion Molecule Deficiencies Increase Porphyromonas gingivalis-Induced Alveolar Bone Loss in Mice

2000 ◽  
Vol 68 (6) ◽  
pp. 3103-3107 ◽  
Author(s):  
Pamela J. Baker ◽  
Lisa DuFour ◽  
Mark Dixon ◽  
Derry C. Roopenian
Keyword(s):  
Bone Resorption ◽  
Bone Loss ◽  
Porphyromonas Gingivalis ◽  
Adhesion Molecule ◽  
Alveolar Bone ◽  
Oral Infection ◽  
Alveolar Bone Loss ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1 ◽  
Complete Deletion

ABSTRACT Alveolar bone resorption can be induced in specific-pathogen-free mice by oral infection with Porphyromonas gingivalis(P. J. Baker, R. T. Evans, and D. C. Roopenian, Arch. Oral Biol. 39:1035–1040, 1994). Here we used a mouse strain, C57BL/6J, which is relatively resistant to P. gingivalis-induced bone loss to examine whether partial or complete deletion of various adhesion molecules would increase susceptibility. Complete deletion of P-selectin or nearly complete lack of expression of intercellular adhesion molecule 1 (ICAM-1) led to increased susceptibility to bone resorption after oral infection, while a hypomorphic defect in β2-integrins did not. Both the total amount of bone lost and the number of sites at which there was significant loss were increased in mice deficient in either ICAM-1 or P-selectin. Each of the three adhesion molecule deficiencies was sufficient to decreaseP. gingivalis-specific serum immunoglobulin G responses, but lower antibody titers did not lead to increased bone loss in partially β2-integrin-deficient mice. In conclusion, P-selectin and ICAM-1 deficiencies increase susceptibility to and severity of alveolar bone loss after P. gingivalisinfection. This finding underscores the importance of innate immunity in protection against P. gingivalis-induced alveolar bone resorption.

scholarly journals Platelet-Activating Factor Receptor Blockade Ameliorates Aggregatibacter actinomycetemcomitans-Induced Periodontal Disease in Mice

2013 ◽  
Vol 81 (11) ◽  
pp. 4244-4251 ◽  
Author(s):  
Mila Fernandes Moreira Madeira ◽  
Celso Martins Queiroz-Junior ◽  
Graciela Mitre Costa ◽  
Silvia Maria Cordeiro Werneck ◽  
Daniel Cisalpino ◽  
...  
Keyword(s):  
Bone Resorption ◽  
Periodontal Disease ◽  
Alveolar Bone ◽  
Platelet Activating Factor ◽  
Aggregatibacter Actinomycetemcomitans ◽  
Content Type ◽  
Periodontal Tissues ◽  
Oral Inoculation ◽  
Paf Receptor

ABSTRACTPeriodontal disease (PD) is a chronic inflammatory and alveolar bone destructive disease triggered by oral biofilm-producing microorganisms, such asAggregatibacter actinomycetemcomitans. The levels of the phospholipid platelet-activating factor (PAF) in the saliva, gingival crevicular fluid, and periodontal tissues are significantly increased during inflammatory conditions, such as PD, but the exact mechanism that links PAF to alveolar bone resorption is not well understood. In the current study, alveolar bone resorption was induced by experimental PD through the oral inoculation ofA. actinomycetemcomitansin wild-type (WT) and PAF receptor knockout (Pafr−/−) mice.In vitroexperiments usingA. actinomycetemcomitanslipopolysaccharide (LPS)-stimulated RAW 264.7 cells treated with a PAF receptor antagonist (UK74505) were also performed. The expression of lyso-PAF acetyltransferase in periodontal tissues was significantly increased 3 h afterA. actinomycetemcomitansLPS injection in mice. WT andPafr−/−mice that were subjected to oral inoculation ofA. actinomycetemcomitanspresented neutrophil accumulation and increased levels of CXCL-1 and tumor necrosis factor alpha (TNF-α) in periodontal tissues. However,Pafr−/−mice presented less alveolar bone loss than WT mice. Thein vitroblockade of the PAF receptor impaired the resorptive activity ofA. actinomycetemcomitansLPS-activated osteoclasts. In conclusion, this study shows for the first time that the blockade of PAF receptor may contribute to the progression of PD triggered byA. actinomycetemcomitansby directly affecting the differentiation and activity of osteoclasts.

scholarly journals Brucella abortus RB51 Induces Protection in Mice Orally Infected with the Virulent Strain B. abortus 2308

2003 ◽  
Vol 71 (5) ◽  
pp. 2326-2330 ◽  
Author(s):  
Paolo Pasquali ◽  
Adone Rosanna ◽  
Claudia Pistoia ◽  
Paola Petrucci ◽  
Franco Ciuchini
Keyword(s):  
Immune Response ◽  
Brucella Abortus ◽  
Protective Immunity ◽  
Virulent Strain ◽  
Oral Route ◽  
Oral Infection ◽  
Virulent Strains ◽  
Cell Mediated Immune Response ◽  
Oral Inoculation ◽  
Common Causes

ABSTRACT Brucellae are gram-negative, facultative intracellular bacteria which are one of the most common causes of abortion in animals. In addition, they are the source of a severe zoonosis. In this trial, we evaluated the effect of oral inoculation of Brucella abortus RB51 in mice against a challenge infection with B. abortus 2308. First, we showed that a gastric acid neutralization prior to the oral inoculation contributed to a more homogeneous and consistent infection with both vaccine strain B. abortus RB51 and virulent strain B. abortus 2308. Successively, we assessed the clearance and the immune response following an oral infection with B. abortus RB51. Oral inoculation gave a mild infection which was cleared 42 days after infection, and it induced a delayed humoral and cell-mediated immune response. Finally, we immunized mice by oral inoculation with B. abortus RB51, and we challenged them with the virulent strain B. abortus 2308 by an oral or intraperitoneal route 42 days after vaccination. Oral inoculation of B. abortus RB51 was able to give protection to mice infected with the virulent strain B. abortus 2308 by the oral route but not to mice infected intraperitoneally. Our results indicate that oral inoculation of mice with B. abortus RB51 is able to give a protective immunity against an oral infection with virulent strains, and this protection seems to rely on an immune response at the mucosal level.

Accelerated Alveolar Bone Loss in Mice Lacking Interleukin-10

2003 ◽  
Vol 82 (8) ◽  
pp. 632-635 ◽  
Author(s):  
A. Al-Rasheed ◽  
H. Scheerens ◽  
D.M. Rennick ◽  
H.M. Fletcher ◽  
D.N. Tatakis
Keyword(s):  
Bone Resorption ◽  
Bone Loss ◽  
Inflammatory Cytokines ◽  
Alveolar Bone ◽  
Interleukin 10 ◽  
Alveolar Bone Loss ◽  
Prevotella Intermedia ◽  
Pro Inflammatory Cytokines

Interleukin-10 regulates pro-inflammatory cytokines, including those implicated in alveolar bone resorption. We hypothesized that lack of interleukin-10 leads to increased alveolar bone resorption. Male interleukin-10(−/−) mice, on 129/SvEv and C57BL/6J background, were compared with age-, sex-, and strain-matched interleukin-10(+/+) controls for alveolar bone loss. Immunoblotting was used for analysis of serum reactivity against bacteria associated with colitis and periodontitis. Interleukin-10(−/−) mice had significantly greater alveolar bone loss than interleukin-10(+/+) mice (p = 0.006). The 30–40% greater alveolar bone loss in interleukin-10(−/−) mice was evident in both strains, with C57BL/6J interleukin-10(−/−) mice exhibiting the most bone loss. Immunoblotting revealed distinct interleukin-10(−/−) serum reactivity against Bacteroides vulgatus, B. fragilis, Prevotella intermedia, and, to a lesser extent, against B. forsythus. The results of the present study suggest that lack of interleukin-10 leads to accelerated alveolar bone loss.

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