Impact of hepcidin antimicrobial peptide on iron overload in tuberculosis patients.

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.