Journal Of Clinical Periodontology · 2020 · 23 citations · 26 references
Life SciencesImmunologyOral BiologyGene ExpressionInflammationInnate ImmunityMicrorna BiologyMicrorna-mediated RegulationPeriodontal DiseasePeriodontal Immune ResponsesPeriodontal ImmunologyPeriodontal InflammationDifferential Expression In MicrornaMicrorna Dysregulation In DiseaseMicrorna GenesMicrorna In Immune RegulationMicrorna In InflammationMicrorna Regulation Of InflammationPeriodontal ImmunopathogenesisPeriodontitis Pathogenesis
AIM: Previous data from our laboratory have demonstrated that localized aggressive periodontitis (LAP) patients produce elevated levels of pro-inflammatory cytokines in response to TLR4 and TLR2 ligation compared to unrelated and periodontally healthy controls (HC). The aim of the present work is to evaluate the contribution of TLR-related gene expression and miRNA regulation in LAP disease. MATERIAL AND METHODS: Peripheral blood mononuclear cells (PBMCs) from LAP and health control (HC) patients were isolated. Gene and miRNA expression involved in TLR signalling pathway and immunopathology were evaluated in unstimulated PBMCs by real-time PCR (RT-PCR). RESULTS: TICAM-1 (TRIF), FOS, IRAK1, TLR2 and CCL2 genes and the miRNAs miR-9-5p, miR-155-5p and 203a-3p, miR-147a, miR-182-5p and miR-183-5p were significantly up-regulated in LAP compared to HC. CONCLUSIONS: Most of the genes and miRNAs overexpressed here are directly or indirectly related to immune response and inflammation. This profile supports our previous findings that suggests LAP patients have a "hyper-responsive" phenotype upon activation of TLR pathway by periodontal pathogens.
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