| Autor: |
Genctoy, Gultekin, Altun, Bulent, Kiykim, Ahmet Alper, Arici, Mustafa, Erdem, Yunus, Ünal Yasavul, Meltem Çaglarg, Turgan, Çetin, Çaglar, Şali |
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| Zdroj: |
Functional Ecology; Feb2015, Vol. 29 Issue 2, p174-178, 5p |
| Abstrakt: |
Background: Renin-angiotensin system (RAS) was suggested to modulate inflammatory cytokine production. Angiotensin II was consistently shown to increase production of tumor necrosis factor alpha (TNF-α). However, inflammatory cytokines and RAS were modulated by genetic polymorphisms such as TNF-α-308 G > A and angiotensin-converting enzyme (ACE) I/D gene polymorphisms. The aim of this study was to investigate the effects of ACE and TNF-α genotypes on inflammatory cytokines in hemodialysis (HD) patients. Methods: ACE I/D and TNF-α-308 G > A genotypes, pre- and postdialysis plasma renin activity (PRA), serum ACE, interleukin-1 beta (IL-1β), and TNF-α levels were determined in 22 HD patients. Results: Predialysis serum ACE activity is correlated with TNF-α (r = 0.63; P = 0.01), and PRA was correlated with IL-1β levels (r = 0.49; P = 0.02). Pre/postdialysis IL-1β and TNF-α were similar in DD and II/ID ACE genotypes. Predialysis TNF-α and IL-1 b (32.4 ± 5; 35.1 ± 4.2 vs. 28.1 ± 3.7; 26.5 ± 6.2 pg/mL; P < 0.05) and postdialysis TNF-α levels (30.4 ± 1.4 vs. 28.4 ± 0.82 pg/mL; P < 0.05) were significantly higher in TNF1/2 than TNF1/1 patients. Conclusion: ACE and TNF-α-308 G > A (1/2) gene polymorphisms may contribute to modulation of proinflammatory cytokine production and hence chronic inflammation in HD patients. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
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