Functional polymorphisms in the gene encoding macrophage migration inhibitory factor (MIF) are associated with active pulmonary tuberculosis

2015 ◽  
Vol 48 (3) ◽  
pp. 222-228 ◽  
Author(s):  
Shou-Gang Kuai ◽  
Qin-Fang Ou ◽  
De-Hong You ◽  
Zhong-Bo Shang ◽  
Jun Wang ◽  
...  
Keyword(s):  
Pulmonary Tuberculosis ◽  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Inhibitory Factor ◽  
Macrophage Migration ◽  
Gene Encoding ◽  
Active Pulmonary Tuberculosis ◽  
Functional Polymorphisms

scholarly journals Association of Vitamin D Receptor Polymorphism (rs2228570, rs1544410, rs7975232, and rs731236) and Macrophage Migration Inhibitory Factor -173 G/C (rs755622) with the Susceptibility of Active Pulmonary Tuberculosis in Makassar, Indonesia

2021 ◽  
Vol 9 (A) ◽  
pp. 838-848
Author(s):  
Najdah Hidayah ◽  
Irawaty Djaharuddin ◽  
Ahyar Ahmad ◽  
Rosdiana Natzir ◽  
Ilhamjaya Patellongi ◽  
...  
Keyword(s):  
Vitamin D ◽  
Pulmonary Tuberculosis ◽  
Vitamin D Receptor ◽  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Active Tuberculosis ◽  
Inhibitory Factor ◽  
Macrophage Migration ◽  
Active Pulmonary Tuberculosis ◽  
Household Contacts

BACKGROUND: The study of Vitamin D Receptor (VDR) and Macrophage Migration Inhibitory Factor (MIF) polymorphisms, associated with active pulmonary tuberculosis (ATB) presents varying results. AIMS: This study aimed to investigate the association between VDR rs2228570, rs1544410, rs7975232, rs731236 and MIF -173 G/C (rs755622) single nucleotide polymorphism (SNP), with susceptibility of developing ATB, and positivity of Interferon Gamma Release Assay (IGRA) results (in household contact). METHODS AND MATERIAL: This study involved 83 ATB and 73 household contacts in Makassar. We checked IGRA based on ELISA in household contacts by using QuantiFERON TB Gold Plus test, and we found that 61.64% (n = 45) of household contacts had positive IGRA. Polymorphism examination was carried out by Sanger sequencing. RESULTS: VDR rs2228570 T/T and T/C-T/T were significantly associated with higher risk of active tuberculosis. VDR rs7975232 G/G genotype was associated with an increased risk of developing active TB compared to T/T-T/G. Haplotype analysis of VDR rs2228570, rs1544410, rs7975232, rs731236 and combination with MIF rs755622 demonstrated that TGGTG was observed to have a higher risk of tuberculosis. CONCLUSIONS: The combination of VDR and MIF variants may contribute to the susceptibility of active tuberculosis disease.

Elevated Levels of Serum Macrophage Migration Inhibitory Factor in Patients with Pulmonary Tuberculosis

2002 ◽  
Vol 104 (2) ◽  
pp. 123-127 ◽  
Author(s):  
Gen Yamada ◽  
Noriharu Shijubo ◽  
Yoko Takagi-Takahashi ◽  
Jun Nishihira ◽  
Yuka Mizue ◽  
...  
Keyword(s):  
Pulmonary Tuberculosis ◽  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Inhibitory Factor ◽  
Macrophage Migration

scholarly journals Macrophage migration inhibitory factor: molecular, cellular and genetic aspects of a key neuroendocrine molecule

2004 ◽  
Vol 182 (1) ◽  
pp. 1-9 ◽  
Author(s):  
RP Donn ◽  
DW Ray
Keyword(s):  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Inflammatory Diseases ◽  
Inhibitory Factor ◽  
Target Cells ◽  
Macrophage Migration ◽  
Signalling Molecules ◽  
Functional Polymorphisms ◽  
Low Concentrations

The immunological and neuroendocrine properties of macrophage migration inhibitory factor (MIF) are diverse. In this article we review the known cellular, molecular and genetic properties of MIF that place it as a key regulatory cytokine, acting within both the innate and adaptive immune responses.The unexpected and paradoxical induction of MIF secretion by low concentrations of glucocorticoids is explored. The role of MIF as a locally acting modulator of glucocorticoid sensitivity within foci of inflammation is also discussed. MIF has no homology with any other pro-inflammatory cytokine and until recently lacked a recognised transmembrane receptor. MIF has also been shown to be directly taken up into target cells and to interact with intracellular signalling molecules, including the Jun activation domain-binding protein Jab-1.Comprehensive analysis of the MIF gene has identified important functional polymorphisms and a series of genetic studies has revealed both association and linkage of MIF with inflammatory diseases. Altered MIF regulation may therefore be pivotal to acquiring chronic inflammation following an innate immune response.

scholarly journals Functional polymorphisms of macrophage migration inhibitory factor as predictors of morbidity and mortality of pneumococcal meningitis

2016 ◽  
Vol 113 (13) ◽  
pp. 3597-3602 ◽  
Author(s):  
Athina Savva ◽  
Matthijs C. Brouwer ◽  
Thierry Roger ◽  
Mercedes Valls Serón ◽  
Didier Le Roy ◽  
...  
Keyword(s):  
Bacterial Meningitis ◽  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Pneumococcal Meningitis ◽  
Inhibitory Factor ◽  
Morbidity And Mortality ◽  
High Expression ◽  
Macrophage Migration ◽  
Systemic Complications ◽  
Functional Polymorphisms

Pneumococcal meningitis is the most frequent and critical type of bacterial meningitis. Because cytokines play an important role in the pathogenesis of bacterial meningitis, we examined whether functional polymorphisms of the proinflammatory cytokine macrophage migration inhibitory factor (MIF) were associated with morbidity and mortality of pneumococcal meningitis. Two functional MIF promoter polymorphisms, a microsatellite (−794 CATT5–8; rs5844572) and a single-nucleotide polymorphism (−173 G/C; rs755622) were genotyped in a prospective, nationwide cohort of 405 patients with pneumococcal meningitis and in 329 controls matched for age, gender, and ethnicity. Carriages of the CATT7 and −173 C high-expression MIF alleles were associated with unfavorable outcome (P = 0.005 and 0.003) and death (P = 0.03 and 0.01). In a multivariate logistic regression model, shock [odds ratio (OR) 26.0, P = 0.02] and carriage of the CATT7 allele (OR 5.12, P = 0.04) were the main predictors of mortality. MIF levels in the cerebrospinal fluid were associated with systemic complications and death (P = 0.0002). Streptococcus pneumoniae strongly up-regulated MIF production in whole blood and transcription activity of high-expression MIF promoter Luciferase reporter constructs in THP-1 monocytes. Consistent with these findings, treatment with anti-MIF immunoglogulin G (IgG) antibodies reduced bacterial loads and improved survival in a mouse model of pneumococcal pneumonia and sepsis. The present study provides strong evidence that carriage of high-expression MIF alleles is a genetic marker of morbidity and mortality of pneumococcal meningitis and also suggests a potential role for MIF as a target of immune-modulating adjunctive therapy.

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