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1.
J Dent Res ; 93(2): 169-74, 2014 Feb.
Artículo en Inglés | MEDLINE | ID: mdl-24334435

RESUMEN

In type 1 diabetes (T1D), a Toll-like receptor (TLR)-hyper-inflammatory monocytic phenotype has been implicated as a mechanism of exacerbated tissue destruction. Other cells of the periodontium, including oral epithelial cells (OECs), express innate immune receptors, including TLRs. To delineate the TLR responses of OECs derived from T1D participants and to determine effects of the anti-inflammatory agent triclosan on the TLR-hyper-inflammatory phenotype, primary human OECs from individuals with T1D and diabetes-free individuals were stimulated with TLR ligands in the presence and/or absence of triclosan. The expression of pro-inflammatory cytokines and micro-RNAs (miRNAs) was evaluated. While the repertoire of TLRs expressed by OECs is similar to that expressed by macrophages (M), the relative amounts and ratios are significantly different. OECs demonstrate a TLR-response profile similar to that of M, yet attenuated. OECs have a unique response to P. gingivalis LPS, where miR146a and miR155 play a regulatory role in responsiveness. OECs from T1D participants are TLR-hyper-responsive, due to dysregulated induction of miR146a and miR155, which is abrogated by pre-treatment with triclosan. The aberrant TLR-activation of OECs in T1D has the potential to contribute to excessive soft- and hard-tissue destruction. Importantly, triclosan's anti-inflammatory property is effective in abrogating TLR-induced OEC hyperactivity.


Asunto(s)
Diabetes Mellitus Tipo 1/inmunología , Mucosa Bucal/inmunología , Receptores Toll-Like/inmunología , Adolescente , Adulto , Anciano , Antiinflamatorios/farmacología , Técnicas de Cultivo de Célula , Células Cultivadas , Células Epiteliales/inmunología , Humanos , Inmunidad Innata/inmunología , Mediadores de Inflamación/análisis , Interleucina-8/análisis , Ligandos , Lipopolisacáridos/inmunología , Macrófagos/inmunología , MicroARNs/análisis , Persona de Mediana Edad , Mucosa Bucal/citología , Fenotipo , Porphyromonas gingivalis/inmunología , Receptor Toll-Like 1/análisis , Receptor Toll-Like 2/análisis , Receptor Toll-Like 4/análisis , Receptor Toll-Like 6/análisis , Factor de Crecimiento Transformador beta1/análisis , Triclosán/farmacología , Adulto Joven
2.
Oral Dis ; 19(3): 296-302, 2013 Apr.
Artículo en Inglés | MEDLINE | ID: mdl-24079913

RESUMEN

UNLABELLED: Periodontal diseases are a class of pathologies wherein oral microbes induce harmful immune responses in a susceptible host. Therefore, an agent that can both reduce microbial burden and lessen pathogenesis of localized inflammation would have beneficial effects in periodontal disease; 2,4,4-trichloro-2-hydroxydiphenyl-ether [triclosan] is currently used in oral care products owing to broad spectrum antimicrobial and anti-inflammatory properties. OBJECTIVE: To determine effects of triclosan on the response of oral epithelial cells to stimulation with the inflammatory microbial product lipopolysaccharide (LPS), a ligand for toll-like receptor 4 [TLR4]. MATERIALS/METHODS: Primary human oral epithelial cells were stimulated with LPS in the presence and/or absence of triclosan after which expression of pro-inflammatory cytokines, ß-defensins, micro-RNAs [miRNAs], or TLR-signaling pathway proteins were evaluated. RESULTS: Here, we demonstrate that triclosan is a potent inhibitor of oral epithelial cell LPS-induced pro-inflammatory responses by inducing miRNA regulation of the TLR-signaling pathway. Triclosan was not a pan-suppresser of oral epithelial cell responses as ß-defensin 2 [ßD2] and ßD3 were upregulated by triclosan following LPS-stimulation. CONCLUSIONS: These data demonstrate both a novel antimicrobial mechanism by which triclosan improves plaque control and an additional anti-inflammatory property, which could have beneficial effects in periodontal disease resolution.


Asunto(s)
Antiinfecciosos/farmacología , Antiinflamatorios/farmacología , Células Epiteliales/efectos de los fármacos , Células Epiteliales/fisiología , Inflamación/prevención & control , Triclosán/farmacología , Células Cultivadas , Humanos , Lipopolisacáridos/farmacología
3.
Oral Dis ; 19(3): 303-12, 2013 Apr.
Artículo en Inglés | MEDLINE | ID: mdl-24079914

RESUMEN

UNLABELLED: Periodontal disease-associated alveolar bone loss is a comorbidity of type-2-diabetes, where the roles of osteoclasts are poorly understood. OBJECTIVE: To evaluate osteoclast differentiation and function in the context of type-2-diabetes. MATERIALS AND METHODS: Bone marrow-derived osteoclasts from db/db mice, a model of type-2-diabetes, as well as human osteoclasts derived from peripheral blood of individuals with type-2-diabetes were evaluated for differentiation, resorption, and soluble mediator expression. RESULTS: While db/db mice were hyperglycemic at time of cell harvest, human participants were glycemically controlled. Although db/db cultures resulted in a higher number of larger osteoclasts, individual cell receptor activator of nuclear factor kappaB ligand (RANKL)-mediated bone resorption was similar to that observed in diabetes-free osteoclasts. Osteoclasts derived from individuals with type-2-diabetes differentiated similarly to controls with again no difference in bone resorbing capacity. Murine and human type-2-diabetes cultures both displayed inhibition of lipopolysaccharide (LPS)-induced deactivation and increased pro-osteoclastogenic mediator expression. CONCLUSIONS: Hyperglycemia plays a role in aberrant osteoclast differentiation leading to an increased capacity for bone resorption. Osteoclasts derived from murine models of and individuals with type-2-diabetes are unable to be inhibited by LPS, again leading to increased capacity for bone resorption. Here, environmental and intrinsic mechanisms associated with the increased alveolar bone loss observed in periodontal patients with type-2-diabetes are described.


Asunto(s)
Diferenciación Celular , Diabetes Mellitus Tipo 2/complicaciones , Hiperglucemia/complicaciones , Osteoclastos/citología , Osteoclastos/fisiología , Animales , Humanos , Ratones
4.
J Dent Res ; 90(9): 1140-4, 2011 Sep.
Artículo en Inglés | MEDLINE | ID: mdl-21730256

RESUMEN

While much research has focused on local and systemic factors contributing to periodontal disease, little is known regarding mechanisms linking these factors. We have previously reported a systemic hyper-inflammatory response to bacterial endotoxin in localized aggressive periodontitis (LAP). The objectives of this study were to delineate cyto/chemokines in gingival crevicular fluid (GCF) and evaluate systemic levels of endotoxin associated with LAP. Clinical parameters, GCF, and peripheral blood were collected from: 34 LAP, 10 healthy siblings, and nine healthy unrelated control individuals. Cyto/chemokines were quantified in GCF, systemic endotoxin levels were quantified in plasma, and correlation analysis was performed among all parameters. Nine mediators were elevated in LAP diseased sites as compared with healthy sites (TNFα, INFγ, IL1ß, IL2, IL6, IL10, Il12p40, GMCSF, and MIP1α, p < 0.001), while MCP1, IL4, and IL8 were elevated in healthy sites (p < 0.01). Four- to five-fold-higher endotoxin levels were detected in LAP plasma compared with that from healthy participants (p < 0.0001), which correlated with all clinical parameters and most cyto/chemokines analyzed. In conclusion, higher systemic levels of endotoxin were found in LAP, which correlates with an exacerbated local inflammatory response and clinical signs of disease. (Clinicaltrials.gov number, NCT01330719).


Asunto(s)
Periodontitis Agresiva/diagnóstico , Biomarcadores , Citocinas/análisis , Líquido del Surco Gingival/química , Lipopolisacáridos/sangre , Proteínas Adaptadoras Transductoras de Señales/análisis , Adolescente , Negro o Afroamericano , Periodontitis Agresiva/sangre , Estudios de Casos y Controles , Niño , Preescolar , Femenino , Factor Estimulante de Colonias de Granulocitos y Macrófagos/análisis , Humanos , Interferón gamma/análisis , Interleucinas/análisis , Masculino , Análisis de Regresión , Estadísticas no Paramétricas , Factor de Necrosis Tumoral alfa/análisis , Adulto Joven
5.
Vet Res ; 31(4): 447-53, 2000.
Artículo en Inglés | MEDLINE | ID: mdl-10958244

RESUMEN

Ultrastructural studies of glomerular changes were performed on 16 pigs experimentally infected with a highly virulent strain of the classical swine fever virus. Our observations revealed the thickening of glomerular basement membranes, swelling of endothelial cells and cytoplasmic vacuolization within podocytes containing abundant viral particles. An early viral infection of podocytes was suggested as the cause of selective swelling of the foot processes of these cells with the consequent obliteration of the glomerular urinary spaces. To our knowledge this is the first report of ultrastructural evidence of classical swine fever virions infecting glomerular podocytes.


Asunto(s)
Peste Porcina Clásica/patología , Glomérulos Renales/ultraestructura , Animales , Virus de la Fiebre Porcina Clásica , Microscopía Electrónica , Porcinos
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