| چکیده انگلیسی مقاله |
Chronic heart failure (CHF) is a complex clinical syndrome that represents the end stage of various cardiac diseases and is characterized by the inability of the heart to meet metabolic demands of the body. Many physiological systems are involved in this disease. In particular, the activation of the immune system has received considerable interest in the last decade. Evidence from both experimental and clinical trials indicates that inflammatory mediators are of importance in the pathogenesis and progression of chronic heart failure. Excessive pro-inflammatory cytokines induce contractile dysfunction, hypertrophy, and fibrosis and cell death in Cardiac myocyte. We examined the expression of IL-23 in PBMCs between CHF patients and healthy controls. In this report, we used real-time PCR assay to compare the relative expression of IL-23 in peripheral blood mononuclear cells (PBMC) from CHF patients with various heart diseases (n=42, EF< 45%, range of New York Heart Association (NYHA) 1 to 4) and matched healthy control subjects (n=42).We also determined the IL-23 concentrations of cell culture supernatant of PBMCs with ELISA. A total of 42 patients with CHF, with 42 age and sex-matched control group subjects were enrolled in the present study. The culture supernatant levels of IL-23 in PBMC of CHF patients were significantly higher (133.95±108.99 pg/mL) than in the control group (83.43±76.2 pg/mL) (P< 0.05). The gene expression of IL-23 was also markedly upregulated in PBMC from CHF patients in comparison with the control group, but it was not statically significant 80. These results demonstrate that in patients with CHF and especially those with severe CHF, expression of pro-inflammatory cytokines and levels of IL-23 cytokine is markedly increased in PBMC. These finding suggested that IL-23 may play an important role in the progression of CHF among these patients. |
| نویسندگان مقاله |
| Vajiheh Eskandari
Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
| Ali Akbar Amirzargar
Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran. AND Molecular Immunology Research Center, Children's Medical Center, Tehran University of Medical Sciences, Tehran, Iran.
| Bobak Moazzami
Student Research Committee, Babol University of Medical Sciences, Babol, Iran. AND Research Center for Immunodeficiencies, Pediatrics Center of Excellence, Children's Medical Center, Tehran University of Medical Sciences, Tehran, Iran.
| Mohammad Jafar Mahmoudi
Department of Cardiology, Amir Alam Hospital, Tehran University of Medical Sciences, Tehran, Iran.
| Zahra Rahnemoon
Cardiac Heart Center, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
| Samaneh Sadati
Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
| Zahra Rahmati
Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
| Fatemeh Gorzin
Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
| Mona Hedayat
Division of Immunology, Boston Children's Hospital, Harvard Medical School, Boston, MA, USA. AND Network of Immunity in Infection, Malignancy and Autoimmunity (NIIMA), Universal Scientific Education and Research Network (USERN), Boston, MA, USA.
| Nima Rezaei
Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran. AND Research Center for Immunodeficiencies, Pediatrics Center of Excellence, Children's Medical Center, Tehran University of Medical Sciences, Tehran, Iran. AND Network of Immunity in Infection, Malignancy and Autoimmunity (NIIMA), Universal Scientific Education and Research Network (USERN), Sheffield, UK.
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