Abstract
PurposeThe establishment of candidate genes associated with susceptibility to TB is a challenge especially due to divergent frequencies among different populations. The objective of this study was to evaluate the association between macrophage migration inhibitory factor (MIF) -173 G>C single nucleotide polymorphism (SNP) and susceptibility to pulmonary TB in a population of southern Brazil.MethodsCase-control study. Patients > 18 years old, diagnosed with pulmonary TB were included. The control group consisted of blood donors and household contacts, not relatives, healthy and > 18 years old. MIF -173 G>C SNPs were genotyped using real-time PCR using a TaqMan SNP Genotyping assay.Results174 patients and 166 controls were included. There were no statistically significant differences between cases and controls regarding genotype prevalence (p>0.05). Comparing patients with normal genotype (GG) with those with at least one C allele, there was also no statistically significant difference (p = 0.135). Also, there was no statistically significant difference comparing the homozygous for the mutation (CC) with the other patients (GG and CG) (p = 0.864).ConclusionsWe did not find association between MIF -173 G>C polymorphism and susceptibility to pulmonary TB.
Highlights
The natural history of tuberculosis (TB) follows a variable course after the initial infection, with only 10% of infected individuals developing clinical disease
There was no statistically significant difference comparing the homozygous for the mutation (CC) with the other patients (GG and CG) (p = 0.864)
The macrophage migration inhibitory factor (MIF) is a cytokine with proinflammatory chemokine-like functions that have been recognized to play a central role in mediating a wide variety of immune responses against invading pathogens, and may be associated with the onset and / or progression of TB
Summary
The natural history of tuberculosis (TB) follows a variable course after the initial infection, with only 10% of infected individuals developing clinical disease. Environmental and bacterial virulence factors can influence the clinical presentation of TB [1]. Many studies indicate that genetic factors play a major role in determining the susceptibility and resistance to TB [2,3,4,5]. Polymorphisms of genes play an important role in the occurrence and development of TB. The macrophage migration inhibitory factor (MIF) is a cytokine with proinflammatory chemokine-like functions that have been recognized to play a central role in mediating a wide variety of immune responses against invading pathogens, and may be associated with the onset and / or progression of TB. A metanalysis revealed a strong association of a MIF polymorphism with autoimmune and infectious diseases [14]. A few studies had evaluated these polymorphisms in TB, in different populations, with controversial results [16,18,19,20,21,22]
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