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Enhancement of Chemokine mRNA Expression by Toll-Like Receptor 2 Stimulation in Human Peripheral Blood Mononuclear Cells of Patients with Atopic Dermatitis

Atopic dermatitis (AD) is a chronic inflammatory skin disease which is often associated with Staphylococcus aureus (S. aureus) colonization. S. aureus ingredients are potential ligands to activate the Toll-like receptor 2 (TLR2) and drive inflammatory cytokine or chemokine production. However, the r...

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Autores principales: Yu, Yangyang, Lin, Dongxu, Cai, Xiaoqiong, Cui, Danni, Fang, Ran, Zhang, Wei, Yu, Bo, Wang, Xiaomei
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7115052/
https://www.ncbi.nlm.nih.gov/pubmed/32280674
http://dx.doi.org/10.1155/2020/1497175
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author Yu, Yangyang
Lin, Dongxu
Cai, Xiaoqiong
Cui, Danni
Fang, Ran
Zhang, Wei
Yu, Bo
Wang, Xiaomei
author_facet Yu, Yangyang
Lin, Dongxu
Cai, Xiaoqiong
Cui, Danni
Fang, Ran
Zhang, Wei
Yu, Bo
Wang, Xiaomei
author_sort Yu, Yangyang
collection PubMed
description Atopic dermatitis (AD) is a chronic inflammatory skin disease which is often associated with Staphylococcus aureus (S. aureus) colonization. S. aureus ingredients are potential ligands to activate the Toll-like receptor 2 (TLR2) and drive inflammatory cytokine or chemokine production. However, the role of TLR2-mediated chemokine expression in AD development has not been systematically investigated. In this study, we sought to determine the mode of TLR2-mediated chemokine expression in AD patients. Human peripheral blood mononuclear cells (PBMCs) were isolated from AD patients and healthy controls. Upon incubation with TLR2 ligands Pam3CSK4 and PGN, mRNA expression of chemokines, including CCL1, CCL5, CCL8, CCL13, CCL17, CCL18, CCL22, and CCL27, were determined by quantitative real-time polymerase chain reaction (qRT-PCR) analysis. The results showed that basal mRNA expression of CCL17 in PBMCs from AD patients was upregulated compared with healthy controls, while those of CCL8 and CCL13 were downregulated. When stimulated with TLR2 ligands, the mRNA expression of CCL5, CCL8, CCL13, CCL18, and CCL22 in PBMCs from AD patients was significantly higher than those from healthy controls. The different basal chemokine mRNA expression profiles indicate the different immune status in patients with AD compared with healthy controls. Excessive chemokine mRNA expression induced by TLR2 activation is associated with the development of AD.
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spelling pubmed-71150522020-04-11 Enhancement of Chemokine mRNA Expression by Toll-Like Receptor 2 Stimulation in Human Peripheral Blood Mononuclear Cells of Patients with Atopic Dermatitis Yu, Yangyang Lin, Dongxu Cai, Xiaoqiong Cui, Danni Fang, Ran Zhang, Wei Yu, Bo Wang, Xiaomei Biomed Res Int Research Article Atopic dermatitis (AD) is a chronic inflammatory skin disease which is often associated with Staphylococcus aureus (S. aureus) colonization. S. aureus ingredients are potential ligands to activate the Toll-like receptor 2 (TLR2) and drive inflammatory cytokine or chemokine production. However, the role of TLR2-mediated chemokine expression in AD development has not been systematically investigated. In this study, we sought to determine the mode of TLR2-mediated chemokine expression in AD patients. Human peripheral blood mononuclear cells (PBMCs) were isolated from AD patients and healthy controls. Upon incubation with TLR2 ligands Pam3CSK4 and PGN, mRNA expression of chemokines, including CCL1, CCL5, CCL8, CCL13, CCL17, CCL18, CCL22, and CCL27, were determined by quantitative real-time polymerase chain reaction (qRT-PCR) analysis. The results showed that basal mRNA expression of CCL17 in PBMCs from AD patients was upregulated compared with healthy controls, while those of CCL8 and CCL13 were downregulated. When stimulated with TLR2 ligands, the mRNA expression of CCL5, CCL8, CCL13, CCL18, and CCL22 in PBMCs from AD patients was significantly higher than those from healthy controls. The different basal chemokine mRNA expression profiles indicate the different immune status in patients with AD compared with healthy controls. Excessive chemokine mRNA expression induced by TLR2 activation is associated with the development of AD. Hindawi 2020-03-19 /pmc/articles/PMC7115052/ /pubmed/32280674 http://dx.doi.org/10.1155/2020/1497175 Text en Copyright © 2020 Yangyang Yu et al. http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Yu, Yangyang
Lin, Dongxu
Cai, Xiaoqiong
Cui, Danni
Fang, Ran
Zhang, Wei
Yu, Bo
Wang, Xiaomei
Enhancement of Chemokine mRNA Expression by Toll-Like Receptor 2 Stimulation in Human Peripheral Blood Mononuclear Cells of Patients with Atopic Dermatitis
title Enhancement of Chemokine mRNA Expression by Toll-Like Receptor 2 Stimulation in Human Peripheral Blood Mononuclear Cells of Patients with Atopic Dermatitis
title_full Enhancement of Chemokine mRNA Expression by Toll-Like Receptor 2 Stimulation in Human Peripheral Blood Mononuclear Cells of Patients with Atopic Dermatitis
title_fullStr Enhancement of Chemokine mRNA Expression by Toll-Like Receptor 2 Stimulation in Human Peripheral Blood Mononuclear Cells of Patients with Atopic Dermatitis
title_full_unstemmed Enhancement of Chemokine mRNA Expression by Toll-Like Receptor 2 Stimulation in Human Peripheral Blood Mononuclear Cells of Patients with Atopic Dermatitis
title_short Enhancement of Chemokine mRNA Expression by Toll-Like Receptor 2 Stimulation in Human Peripheral Blood Mononuclear Cells of Patients with Atopic Dermatitis
title_sort enhancement of chemokine mrna expression by toll-like receptor 2 stimulation in human peripheral blood mononuclear cells of patients with atopic dermatitis
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7115052/
https://www.ncbi.nlm.nih.gov/pubmed/32280674
http://dx.doi.org/10.1155/2020/1497175
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