Dysregulation of genes and microRNAs in localized aggressive periodontitis

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...

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Bibliographic Details
Published in:Journal of clinical periodontology 2020-11, Vol.47 (11), p.1317-1325
Main Authors: Gonçalves Fernandes, Jussara, Morford, Lorri Ann, Harrison, Peter Lloyd, Kompotiati, Theodora, Huang, Hong, Aukhil, Ikramuddin, Wallet, Shannon Margaret, Macchion Shaddox, Luciana
Format: Article
Language:English
Subjects:
Aggressive Periodontitis - genetics
Cytokines
Dentistry
Gene expression
Gene Expression Profiling
Gum disease
Humans
Immune response
Inflammation
IRAK protein
Leukocytes, Mononuclear
MicroRNAs
MicroRNAs - genetics
miRNA
Monocyte chemoattractant protein 1
Periodontitis
Peripheral blood mononuclear cells
Phenotypes
Signal Transduction
TLR2 protein
TLR4 protein
Toll-like receptors
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Summary: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.
ISSN:0303-6979
1600-051X
DOI:10.1111/jcpe.13361