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ORIGINAL ARTICLE
Year : 2019  |  Volume : 21  |  Issue : 3  |  Page : 161-166

Are thermogenic proteins and adipokine chemerin affected by monoclonal antibody therapy in asthma?


1 Department of Pathology, Antalya Education and Research Hospital, Antalya, Turkey
2 Department of Internal Medicine, Allergy and Clinical Immunology, Academia Sinica, Genomics Research Center, Taipei, Taiwan; Department of Internal Medicine, Allergy and Clinical Immunology, Antalya Education and Research Hospital, Antalya, Turkey
3 Department of Medical Biochemistry, Faculty of Medicine, Akdeniz University, Antalya, Turkey
4 Department of Medical Biochemistry, Faculty of Medicine, Bozok University, Yozgat, Turkey

Correspondence Address:
Prof. Arzu Didem Yalcin
Internal Medicine, Allergy and Clinical Immunology, Academia Sinica, Genomics Research Center, 11529 Taipei, Taiwan; Internal Medicine, Allergy and Clinical Immunology, Antalya Education and Research Hospital, Antalya, Turkey

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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ejop.ejop_60_18

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BACKGROUND: Irisin is a thermogenic protein that sources outgoing energy by converting white adipose tissue to brown adipose tissue. Chemerin is originally identified as a chemoattractant protein that mainly mediating the chemotaxis of dendritic cells and natural killer cells (NKCs). The aim of this study is to assess the potential impact of immune modulation-related chemerin and irisin concentrations together with cell surface markers (CSM) in allergic asthmatic patients under omalizumab treatment. MATERIALS AND METHODS: The study participants were age- and sex-matched 30 healthy controls (Group I) and consecutive patients who had severe persistent asthma disease (Group II). Asthma patients took omalizumab treatment for 12 months within every 2 weeks. Flow cytometry analysis was used to evaluate CSM, enzyme-linked immunosorbent assay (ELISA) for interleukin-1 (IL-1) β expression. In addition, NK activity (NKA) and induced cytokine expression (by bioassay and ELISA, respectively) before and after omalizumab therapy were evaluated. RESULTS: Chemerin, irisin, and IL-1 β concentrations were significantly higher in severe persistent asthma patients compared to controls in serum (P = 0.01; P = 0.03; and P = 0.008, respectively). IL-1 β level decreased with treatment and it was statistically significant. Although levels decreased, no statistically significant difference was observed for Irisin, CD80, and CD56/16 levels. Chemerin level kept rising after treatment, and this was significant statistically. CONCLUSIONS: This is the first study to assess NKA and adipokines in asthma patients and their relationship with CSM. We observed that the level of these molecules is higher in asthma and is influenced by omalizumab treatment. Since no obvious change was observed for NKCs, omalizumab may be considered safe against cancer development.


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