Dysregulation of genes and microRNAs in localized aggressive periodontitis

Jussara Gonçalves Fernandes; Lorri Ann Morford; Peter Lloyd Harrison; Theodora Kompotiati; Hong Huang; Ikramuddin Aukhil; Shannon Margaret Wallet; Luciana Macchion Shaddox

doi:10.1111/jcpe.13361

Dysregulation of genes and microRNAs in localized aggressive periodontitis

Jussara Gonçalves Fernandes, Lorri Ann Morford, Peter Lloyd Harrison, Theodora Kompotiati, Hong Huang, Ikramuddin Aukhil, Shannon Margaret Wallet, Luciana Macchion Shaddox

Oral Health Science

Research output: Contribution to journal › Article › peer-review

18 Scopus citations

Abstract

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.

Original language	English
Pages (from-to)	1317-1325
Number of pages	9
Journal	Journal of Clinical Periodontology
Volume	47
Issue number	11
DOIs	https://doi.org/10.1111/jcpe.13361
State	Published - Nov 1 2020

Bibliographical note

Publisher Copyright:
© 2020 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd

Funding

This research was supported by National Institute of Health/National Institute of Dental and Craniofacial Research (NIH/NIDCR R01DE019456). The authors would like to thank the doctors and staff at the Leon (Drs. John Bidwell, Edward Zapert and Dan Cober) and Duval County Health Department (Drs Phillis Varnado and Renata Sturtz) dental centres for their assistance in coordinating our visits to their clinics, patient referrals and dental care. This study is registered in Clinicaltrials.gov (#NCT01330719). This research was supported by National Institute of Health/National Institute of Dental and Craniofacial Research (NIH/NIDCR R01DE019456).

Funders	Funder number
Department of Health, Duval County	01330719
National Institutes of Health (NIH)
National Institute of Dental and Craniofacial Research	R01DE019456
National Institute of Dental and Craniofacial Research

ASJC Scopus subject areas

Periodontics

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10.1111/jcpe.13361

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title = "Dysregulation of genes and microRNAs in localized aggressive periodontitis",

abstract = "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.",

author = "\{Gon{\c c}alves Fernandes\}, Jussara and Morford, \{Lorri Ann\} and Harrison, \{Peter Lloyd\} and Theodora Kompotiati and Hong Huang and Ikramuddin Aukhil and Wallet, \{Shannon Margaret\} and \{Macchion Shaddox\}, Luciana",

note = "Publisher Copyright: {\textcopyright} 2020 John Wiley \& Sons A/S. Published by John Wiley \& Sons Ltd",

year = "2020",

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doi = "10.1111/jcpe.13361",

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AU - Gonçalves Fernandes, Jussara

AU - Morford, Lorri Ann

AU - Harrison, Peter Lloyd

AU - Kompotiati, Theodora

AU - Huang, Hong

AU - Aukhil, Ikramuddin

AU - Wallet, Shannon Margaret

AU - Macchion Shaddox, Luciana

PY - 2020/11/1

Y1 - 2020/11/1

N2 - 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.

AB - 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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Dysregulation of genes and microRNAs in localized aggressive periodontitis

Abstract

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