Transcription Factors Regulating Inflammatory Cytokine Production Are Differentially Expressed in Peripheral Blood Mononuclear Cells of Behçet Disease Depending on Disease Activity.
- Author:
Min Yeong WOO
1
;
Su Jin YUN
;
Mi Jin LEE
;
Kyongmin KIM
;
Eun So LEE
;
Sun PARK
Author Information
- Publication Type:Original Article
- Keywords: Behcet syndrome; CCAAT-enhancer-binding proteins; Gene expression; Interleukin-6; Tumor necrosis factor-alpha
- MeSH: Activating Transcription Factor 3; Behcet Syndrome*; Blotting, Western; CCAAT-Enhancer-Binding Proteins; Cytokines; Enzyme-Linked Immunosorbent Assay; Gene Expression; Humans; Interleukin-6; Interleukins; RNA, Small Interfering; Transcription Factors*; Tumor Necrosis Factor-alpha
- From:Annals of Dermatology 2017;29(2):173-179
- CountryRepublic of Korea
- Language:English
- Abstract: BACKGROUND: Behçet disease (BD) is a relapsing inflammatory disease with increased production of inflammatory cytokines in peripheral blood mononuclear cells (PBMCs); however, the underlying molecular mechanisms are not well known. OBJECTIVE: To analyze whether the differential expression of transcription factors is involved in the increased tumor necrosis factor (TNF)-α and interleukin (IL)-6 production by PBMCs of BD patients compared to healthy controls (HCs). METHODS: Expression of transcription factors was examined by real-time reverse transcriptase-polymerase chain reaction and western blotting. Cytokine production by CD11b+ cells transfected with siRNAs against transcription factors was measured by enzyme-linked immunosorbent assay. RESULTS: In the absence of lipopolysaccharide stimulation, the transcript level of CCAAT-enhancer-binding proteins (C/EBP) β was increased in PBMCs from patients with active BD compared to that in PBMCs from patients with stable BD. The C/EBPδ transcript level was higher in PBMCs from patients with active BD than in those from HCs. The activating transcription factor 3 (ATF3) transcript level was increased in PBMCs from patients with stable BD compared to that in PBMCs from HCs. siRNAs targeting C/EBPβ and C/EBPδ significantly reduced the production of IL-6 and TNF-α in lipopolysaccharide-stimulated CD11b+ cells from patients with BD as well as from HCs. CONCLUSION: We found differential expression of C/EBPβ, C/EBPδ, and ATF3 in PBMCs from patients with BD depending on disease activity, indicating the involvement of these molecules in BD pathogenesis.
