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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Published in | Journal of clinical periodontology Vol. 47; no. 11; pp. 1317 - 1325 |
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Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
Blackwell Publishing Ltd
01.11.2020
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Subjects | |
Online Access | Get full text |
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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. |
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Bibliography: | Funding information This research was supported by National Institute of Health/National Institute of Dental and Craniofacial Research (NIH/NIDCR R01DE019456). ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0303-6979 1600-051X |
DOI: | 10.1111/jcpe.13361 |