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

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  • Additional Information
    • Source:
      Publisher: Hindawi Pub. Co Country of Publication: United States NLM ID: 101600173 Publication Model: eCollection Cited Medium: Internet ISSN: 2314-6141 (Electronic) NLM ISO Abbreviation: Biomed Res Int Subsets: MEDLINE
    • Publication Information:
      Original Publication: New York, NY : Hindawi Pub. Co.
    • Subject Terms:
    • Abstract:
      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.
      Competing Interests: The authors declare no commercial or financial conflict of interest.
      (Copyright © 2020 Yangyang Yu et al.)
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    • Accession Number:
      0 (CCL13 protein, human)
      0 (CCL17 protein, human)
      0 (CCL18 protein, human)
      0 (CCL22 protein, human)
      0 (CCL27 protein, human)
      0 (Chemokine CCL17)
      0 (Chemokine CCL22)
      0 (Chemokine CCL27)
      0 (Chemokines)
      0 (Chemokines, CC)
      0 (Cytokines)
      0 (Monocyte Chemoattractant Proteins)
      0 (RNA, Messenger)
      0 (TLR2 protein, human)
      0 (Toll-Like Receptor 2)
    • Publication Date:
      Date Created: 20200414 Date Completed: 20210107 Latest Revision: 20210107
    • Publication Date:
      20231215
    • Accession Number:
      PMC7115052
    • Accession Number:
      10.1155/2020/1497175
    • Accession Number:
      32280674