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Year : 2015  |  Volume : 4  |  Issue : 1  |  Page : 218

2,3,7,8-tetrachlorodibenzo-p-dioxin decrease expression of aryl hydrocarbon receptor in peripheral lymphocyte of β-thalassemia major patients

1 Department of Immunology, School of Medicine, Isfahan University of Medical Sciences, Isfahan; Department of Stem Cell Biology, Stem Cell Technology Research Center Tarbiat Modares University, Tehran, Iran
2 Department of Hematology, Tarbiat Modares University, Tehran, Iran
3 Department of Immunology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran
4 Department of Immunology, School of Medicine, Shahrekord University of Medical Sciences, Shahrekord, Iran

Correspondence Address:
Minoo Adib
Department of Immunology, School of Medicine, Isfahan University of Medical Sciences, Isfahan
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Source of Support: Isfahan University of Medical Science, Conflict of Interest: None declared.

DOI: 10.4103/2277-9175.166165

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Background: β-thalassemia major is a hereditary disease with inefficient erythropoiesis. Level of inflammatory cytokine is elevated in these patients. In this study, we investigate the effect of aryl hydrocarbon receptor (AhR) ligand, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), on the expression of inflammatory mediators in β-thalassemia major patient's lymphocytes. Materials and Methods: Peripheral blood mononuclear cells of patients and healthy participants was isolated and cultured in favor of lymphocytes increment. Based on the treatment, we divided the cell into four groups. The orders of group's treatments were no treatment, tumor necrosis factor-α (TNF-α) treatment, TNF-α and TCDD treatment, TCDD treatment in Group 1–4, respectively. After cell culture, we extracted the cells RNA and converted them to cDNA. Real-time polymerase chain reaction was performed to assessment relative expression of caspase-1, NLRP3, and AhR. We compared all patient groups with equal healthy (control) groups. Results: Results showed that expression of caspase-1 in patients (Groups 1 and 2) was significantly lower than healthy individuals (P < 0.05). Although, no significant difference was found (Groups 1, 2, and control) in AhR gene expression (P > 0.05). Expression of AhR in other groups of patients (3 and 4) was significantly lower than control groups (P < 0.05). Expression of caspase-1 in Group 4 was significantly larger than the control group (P < 0.001). Conclusions: We show here that chronic inflammation decrease caspase-1 expression and exposure of human lymphocytes to TCDD promote caspase-1 expression. Furthermore, activation of AhR with TCDD decreases AhR expression in lymphocytes of β-thalassemia major disease.

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