Association between genetic variants of TLR2, TLR4, TLR9 and schizophrenia.

Schizophrenia Schizophrénie TLR2 TLR4 TLR9 Variants

Journal

L'Encephale
ISSN: 0013-7006
Titre abrégé: Encephale
Pays: France
ID NLM: 7505643

Informations de publication

Date de publication:
15 Sep 2023
Historique:
received: 20 02 2023
revised: 23 05 2023
accepted: 23 05 2023
medline: 18 9 2023
pubmed: 18 9 2023
entrez: 17 9 2023
Statut: aheadofprint

Résumé

Schizophrenia (SZ) is a multifactorial disorder involving complex interactions between genetic and environmental factors, where immune dysfunction plays a key etiopathogenic role. In order to explore the control of innate immune responses in SZ, we aimed to investigate the potential association between twelve TLR2, TLR4 and TLR9 variants (TLR2: rs4696480T>A, rs3804099T>C, rs3804100T>C; TLR4: rs1927914G>A, rs10759932T>C, rs4986790A>G, rs4986791T>C, rs11536889G>C, rs11536891T>C; TLR9: rs187084A>G, rs352139T>C and rs352140C>T) and SZ susceptibility in a Tunisian population. This study included 150 patients and 201 healthy controls with no history of psychiatric illness. Genotyping was done using a TaqMan SNP genotyping assay. We also assessed a haplotype analysis for TLR2, TLR4 and TLR9 variants with SZ using Haploview 4.2 Software. We found that the AA genotype of the TLR2 rs4696480T>A variant was significantly associated with an increased risk of SZ (46% vs. 31%, P=4.7×10 The results indicate that TLR2 and TLR9 genetic diversity may play a role in genetic vulnerability to SZ. However, including more patients and evaluation of TLR2 and TLR9 expression are recommended.

Sections du résumé

BACKGROUND AND STUDY AIM OBJECTIVE
Schizophrenia (SZ) is a multifactorial disorder involving complex interactions between genetic and environmental factors, where immune dysfunction plays a key etiopathogenic role. In order to explore the control of innate immune responses in SZ, we aimed to investigate the potential association between twelve TLR2, TLR4 and TLR9 variants (TLR2: rs4696480T>A, rs3804099T>C, rs3804100T>C; TLR4: rs1927914G>A, rs10759932T>C, rs4986790A>G, rs4986791T>C, rs11536889G>C, rs11536891T>C; TLR9: rs187084A>G, rs352139T>C and rs352140C>T) and SZ susceptibility in a Tunisian population.
PATIENTS AND METHODS METHODS
This study included 150 patients and 201 healthy controls with no history of psychiatric illness. Genotyping was done using a TaqMan SNP genotyping assay. We also assessed a haplotype analysis for TLR2, TLR4 and TLR9 variants with SZ using Haploview 4.2 Software.
RESULTS RESULTS
We found that the AA genotype of the TLR2 rs4696480T>A variant was significantly associated with an increased risk of SZ (46% vs. 31%, P=4.7×10
CONCLUSION CONCLUSIONS
The results indicate that TLR2 and TLR9 genetic diversity may play a role in genetic vulnerability to SZ. However, including more patients and evaluation of TLR2 and TLR9 expression are recommended.

Identifiants

pubmed: 37718198
pii: S0013-7006(23)00114-8
doi: 10.1016/j.encep.2023.05.004
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Informations de copyright

Copyright © 2023 L'Encéphale, Paris. Published by Elsevier Masson SAS. All rights reserved.

Auteurs

Fayza Ayari (F)

Clinical Biology Department, Salah Azaiz Institute, Tunis, Tunisia; Faculty of Sciences of Tunis, University Tunis El Manar, Tunis, Tunisia. Electronic address: fayzaayari09@gmail.com.

Arij Ben Chaaben (AB)

Biology Department, Higher School of Health Sciences and Techniques, Tunis El Manar University, Tunis, Tunisia; Human Genetic Laboratory (LR99E510), Faculty of Medicine, University of Tunis El Manar, Tunis, Tunisia.

Hajer Abaza (H)

Research Unit 03/04 Schizophrenia and Department of Psychiatry F, Razi Hospital, Manouba, Tunisia.

Ons Mihoub (O)

Human Genetic Laboratory (LR99E510), Faculty of Medicine, University of Tunis El Manar, Tunis, Tunisia.

Nesrine Ouni (N)

Clinical Biology Department, Salah Azaiz Institute, Tunis, Tunisia; Faculty of Sciences of Tunis, University Tunis El Manar, Tunis, Tunisia.

Wahid Boukouaci (W)

Université Paris Est Creteil (UPEC), INSERM, IMRB, Translational Neuropsychiatry, Fondation FondaMental, 94010 Creteil, France.

Maher Kharrat (M)

Human Genetic Laboratory (LR99E510), Faculty of Medicine, University of Tunis El Manar, Tunis, Tunisia.

Marion Leboyer (M)

Université Paris Est Creteil (UPEC), INSERM, IMRB, Translational Neuropsychiatry, Fondation FondaMental, 94010 Creteil, France.

Fethi Guemira (F)

Clinical Biology Department, Salah Azaiz Institute, Tunis, Tunisia.

Ryad Tamouza (R)

Université Paris Est Creteil (UPEC), INSERM, IMRB, Translational Neuropsychiatry, Fondation FondaMental, 94010 Creteil, France.

Amani Mankai (A)

Biology Department, Higher School of Health Sciences and Techniques, Tunis El Manar University, Tunis, Tunisia; Research Unit "Obesity: etiopathology and treatment, UR18ES01", National Institute of Nutrition and Food Technology, Tunis, Tunisia.

Classifications MeSH