Mina Javaheri-Kermani, Touraj Farazmandfar, Abolghasem Ajami, Yaghoub Yazdani
{"title":"抗菌肽hepcidin对结核患者铁超载的影响。","authors":"Mina Javaheri-Kermani, Touraj Farazmandfar, Abolghasem Ajami, Yaghoub Yazdani","doi":"10.3109/00365548.2014.929736","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>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.</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>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).</p><p><strong>Conclusion: </strong>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.</p>","PeriodicalId":21541,"journal":{"name":"Scandinavian Journal of Infectious Diseases","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2014-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3109/00365548.2014.929736","citationCount":"16","resultStr":"{\"title\":\"Impact of hepcidin antimicrobial peptide on iron overload in tuberculosis patients.\",\"authors\":\"Mina Javaheri-Kermani, Touraj Farazmandfar, Abolghasem Ajami, Yaghoub Yazdani\",\"doi\":\"10.3109/00365548.2014.929736\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>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.</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>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).</p><p><strong>Conclusion: </strong>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.</p>\",\"PeriodicalId\":21541,\"journal\":{\"name\":\"Scandinavian Journal of Infectious Diseases\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2014-10-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.3109/00365548.2014.929736\",\"citationCount\":\"16\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Scandinavian Journal of Infectious Diseases\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.3109/00365548.2014.929736\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2014/8/19 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Scandinavian Journal of Infectious Diseases","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.3109/00365548.2014.929736","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2014/8/19 0:00:00","PubModel":"Epub","JCR":"","JCRName":"","Score":null,"Total":0}
Impact of hepcidin antimicrobial peptide on iron overload in tuberculosis patients.
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.