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Modulating toll-like receptor-mediated inflammatory responses following exposure of whole cell and lipopolysaccharide component from Porphyromonas gingivalis in wistar rat models

OBJECTIVE: To explore host innate inflammatory response and the signal pathway induced by Porphyromonas gingivalis by measuring level of toll-like receptor 2 (TLR2) and TLR4 activity. MATERIALS AND METHODS: Animal experimental study with pretest-posttest controlled group design were done between Jan...

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Detalles Bibliográficos
Autores principales: Nelwan, Sindy Cornelia, Nugraha, Ricardo Adrian, Endaryanto, Anang, Retno, Indrawati
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Medknow Publications & Media Pvt Ltd 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5727724/
https://www.ncbi.nlm.nih.gov/pubmed/29279665
http://dx.doi.org/10.4103/ejd.ejd_147_17
Descripción
Sumario:OBJECTIVE: To explore host innate inflammatory response and the signal pathway induced by Porphyromonas gingivalis by measuring level of toll-like receptor 2 (TLR2) and TLR4 activity. MATERIALS AND METHODS: Animal experimental study with pretest-posttest controlled group design were done between January 1 and December 10, 2016.. Total of 28 wistar rats had been used, randomized into 7 groups, each were given various dose of intra-sulcural injection of Porphyromonas gingivalis lipopolysaccharide. STATISTICAL ANALYSIS: Normality were measured by Shapiro–Wilk test, while statistical analysis made by ANOVA, t test, Pearson, and linear regression model.. RESULTS: At day 0, no significant difference TLR2 and TLR4 level were measured. At day 4, there is a slight difference between TLR2 and TLR4 level in each group. At day 11, there is a significant difference between TLR2 and TLR4 level in each group. Group with exposure of whole cell will develop greater TLR2 but lower TLR4 level. In the contrary, group with exposure of LPS will develop greater TLR4 but lower TLR2 level. CONCLUSION: Our data supported that P. gingivalis played a vital role in the pathogenesis of pathogen-induced inflammatory responses in which TLR2 and TLR4 have different molecular mechanisms following recognition of pathogens and inflammatory response.