Abstract
Background: Iron acquisition is essential for the growth of Mycobacterium tuberculosis. Hepcidin is known as an antimicrobial peptide and a component of the innate immune response. Hepcidin inhibits M. tuberculosis growth in vitro. In this study, we decided to identify −582A> G variants of the HAMP promoter in patients with tuberculosis (TB) and investigate its effect on serum iron, ferritin, and hepcidin levels. Methods: The sample population consisted of 105 patients with TB and 104 healthy individuals. The −582A> G polymorphism was genotyped using a tetra-primers PCR set. Serum levels of hepcidin were determined using an ELISA kit. Statistical analysis was performed using SPSS software. Results: The G allele is meaningfully associated with TB disease (95% confidence interval = 2–4.8, p < 0.000). Significant differences were seen in the levels of serum iron and hepcidin but not ferritin between the −582A>G polymorphism genotypes. There was significant reverse correlation between hepcidin and iron (r = −0.849, p = 0.006). Conclusion: A high association was found between serum hepcidin levels and the HAMP −582A> G variants in patients with TB. These observations indicate a hypothetical role of this polymorphism in iron metabolism. Hepcidin could perhaps be an option for the treatment of TB.
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Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.
This study was prepared from Mina Javaheri- Kermani's MSc thesis and supported by grants from Golestan University of Medical Sciences and Mazandaran University of Medical Sciences.