Abstract

Background: Elevated levels of circulating Resistin, a peptide hormone produced by adipocytes in rodents but also by monocytes and macrophages in humans, has been reported in patients with tuberculosis infection. To date, only a few studies mainly focused in conditions such as diabetes, obesity, and cardio-metabolic risk have treated to analyse the role of single nucleotide polymorphisms in the Resistin Gene (RETN). However, polymorphisms in this gene have not been previously tested in pulmonary tuberculosis susceptibility. Methods: The rs1862513 (-420C>G), a functional polymorphism in the RETN gene, which has been found to increase circulating resistin levels, was analysed in 192 patients with pulmonary tuberculosis, all of them HIV negative, and in 245 healthy individuals from a well genetically conserved Spanish population. Results: Significant differences in genotype and allele frequencies of the rs1862513 functional polymorphism were not observed between patients and normal controls. Conclusion: Our results would indicate that RETN rs1862513 would not play a major role in the susceptibility to pulmonary tuberculosis at least in our population in a well-powered study.

Highlights

  • Tuberculosis (TB) is still a leading cause of death in humans and remains a global health problem

  • 10% of individuals infected with Mycobacterium tuberculosis (MTB) develop active pulmonary disease, suggesting that there exist differences in susceptibility or resistance to progression

  • Due to the lack of previous studies regarding the role of this Single Nucleotide Polymorphism (SNP) in pulmonary TB (PTB), the aim of this work was to elucidate if this SNP could be Mycobact Dis ISSN:2161-1068 MDTL, an open access journal

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Summary

Introduction

Tuberculosis (TB) is still a leading cause of death in humans and remains a global health problem. Mycobacterium tuberculosis (MTB) infects approximately one-third of the human population. 10% of individuals infected with MTB develop active pulmonary disease, suggesting that there exist differences in susceptibility or resistance to progression. Elevated levels of circulating Resistin, a peptide hormone produced by adipocytes in rodents and by monocytes and macrophages in humans, has been reported in patients with tuberculosis infection. Only a few studies mainly focused in conditions such as diabetes, obesity, and cardio-metabolic risk have treated to analyse the role of single nucleotide polymorphisms in the Resistin Gene (RETN). Polymorphisms in this gene have not been previously tested in pulmonary tuberculosis susceptibility

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