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Altered Systemic Adipokines in Patients with Chronic Urticaria

Authors
Trinh, HK | Pham, DL | Ban, GY  | Lee, HY | Park, HS  | Ye, YM
Citation
International archives of allergy and immunology, 171(2). : 102-110, 2016
Journal Title
International archives of allergy and immunology
ISSN
1018-24381423-0097
Abstract
BACKGROUND: Increasing evidence suggests that adipokines affect immune responses and chronic urticaria (CU) is associated with an altered immune response related to chronic systemic inflammation. Our objectives were to investigate whether adipokines are involved in CU pathogenesis and to outline relationships between adipokines and urticaria severity and quality of life. METHODS: Serum adiponectin, leptin, lipocalin-2 (LCN2), interleukin (IL)-10, IL-6, and tumor necrosis factor (TNF)-alpha concentrations were measured by enzyme-linked immunosorbent assays in 191 CU patients and 89 healthy controls. The effect of LCN2 on N-formyl-methionine-leucine-phenylalanine (fMLP)-induced neutrophil chemotaxis was assessed using migration assays. CU severity was assessed based on the urticaria activity score (UAS). To explore relationships between adipokines and UAS and the chronic urticaria-specific quality of life (CU-QoL) questionnaire, a structural equation model was used. RESULTS: Mean levels of serum LCN2, TNF-alpha, IL-6, and IL-10 were significantly higher in CU patients than in controls. Adiponectin levels were significantly lower in patients with CU than in controls. While serum IL-6 levels were significantly higher in refractory CU patients, compared to responsive CU individuals, LCN2 levels were significantly lower. LCN2 inhibited fMLP-induced neutrophil migration. LCN2 showed a direct relationship with UAS (beta = -0.274, p < 0.001), and UAS was found to contribute to CU-QoL (beta = 0.417, p < 0.001). CONCLUSIONS: Our results highlighted an imbalance in pro- and anti-inflammatory adipokines in CU patients. We suggest that LCN2 could be a differential marker for disease activity and the clinical responses to antihistamine treatment in CU patients. Modulation of systemic inflammation may be a therapeutic strategy for treating severe, refractory CU.
MeSH

DOI
10.1159/000452626
PMID
27902979
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Allergy
Ajou Authors
박, 해심  |  반, 가영  |  예, 영민
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