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FOR AUTHORS Bratislava Medical Journal 2017 Bratislava Medical Journal Vol.118, No.10, p.637-641, 2017
FOR AUTHORS Bratislava Medical Journal 2017 Bratislava Medical Journal Vol.118, No.10, p.637-641, 2017
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Bratislava Medical Journal Vol.118, No.10, p.637-641, 2017 |
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| Title: FOXP3, RORγt and IL-10 cytokine profile in chronic heart failure | ||
| Author: F. Gorzin, A. A. Amirzargar, M. J. Mahmoudi, Z. Rahnemoon, F. Najmi Varzaneh, M. Hedayat, S. Sadati, V. Eskandari, Z. Rahmati, N. Rezaei | ||
| Abstract: BACKGROUND: Distinct subsets of T cells play crucial regulatory roles in inflammatory processes of chronic heart failure (CHF). Retinoic acid receptor-related orphan receptor-γt (Ror-γt) and Forkhead box P3 (Foxp3) have been defined as the “master regulators” of Th17 cells and Treg cells, respectively. At the same time, anti-inflammatory cytokines such as IL-10 may neutralize inflammation in CHF. The current study was designed to compare FOXP3, RORγt and IL-10 protein expression in the blood and IL-10 in supernatant PBMCs in CHF patients versus normal subjects. PATIENTS AND METHODS: Our study population consisted of 42 patients with CHF in four different function classes and 42 healthy subjects who served as controls. RNA extraction and cDNA synthesis was performed and mRNA expression for genes FOXP3, RORγt, IL-10 was determined by RT-PCR. The amount of IL-10 protein in supernatant of PBMCs was measured by ELISA technique. RESULTS: There was no significant difference in FOXP3, RORγt, IL-10 protein expression and supernatant PBMCs IL-10 in CHF patients as compared to control. The level of Foxp3 was significantly lower in CHF patients with ischemic vs non-ischemic cause (p = 0.04). DISCUSSION: Although inflammation plays a central role in the pathophysiology of CHF, the roles of FOXp3, RORγt, and IL-10 remain to be determined (Tab. 3, Ref. 33). |
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| Keywords: CHF, inflammation, FOXP3, RORγt, IL-10 | ||
| Published online: 13-Nov-2017 | ||
| Year: 2017, Volume: 118, Issue: 10 | Page From: 637, Page To: 641 | |
| doi:10.4149/BLL_2017_122 |
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