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Macrophage migrating inhibitory factor expression is associated with Trypanosoma brucei gambiense infection and is controlled by trans-acting expression quantitative trait loci in the Guinean population. | LitMetric

Macrophage migrating inhibitory factor expression is associated with Trypanosoma brucei gambiense infection and is controlled by trans-acting expression quantitative trait loci in the Guinean population.

Infect Genet Evol

Ministère de la Santé et de l'Hygiène Publique, Programme National de Lutte contre la Trypanosomiase Humaine Africaine (PNLTHA), Conakry, Guinea; Institut de Recherche pour le Développement (IRD), UMR IRD-CIRAD 177 INTERTRYP, Montpellier, France. Electronic address:

Published: July 2019

AI Article Synopsis

  • - Infection with Trypanosoma brucei gambiense shows a range of clinical outcomes, and this study explored the link between macrophage migrating inhibitory factor (MIF), an important immune system protein, and disease severity.
  • - Researchers found significantly higher MIF levels in infected individuals and those with latent infections compared to healthy controls, and levels dropped after treatment.
  • - The study identified 4 genetic regions that could regulate MIF expression, highlighting that while MIF is elevated in infected humans, it does not seem to cause disease symptoms.

Article Abstract

Infection by Trypanosoma brucei gambiense is characterized by a wide array of clinical outcomes, ranging from asymptomatic to acute disease and even spontaneous cure. In this study, we investigated the association between macrophage migrating inhibitory factor (MIF), an important pro-inflammatory cytokine that plays a central role in both innate and acquired immunity, and disease outcome during T. b. gambiense infection. A comparative expression analysis of patients, individuals with latent infection and controls found that MIF had significantly higher expression in patients (n = 141; 1.25 ± 0.07; p < .0001) and latent infections (n = 25; 1.23 ± 0.13; p = .0005) relative to controls (n = 46; 0.94 ± 0.11). Furthermore, expression decreased significantly after treatment (patients before treatment n = 33; 1.40 ± 0.18 versus patients after treatment n = 33; 0.99 ± 0.10, p = .0001). We conducted a genome wide eQTL analysis on 29 controls, 128 cases and 15 latently infected individuals for whom expression and genotype data were both available. Four loci, including one containing the chemokine CXCL13, were found to associate with MIF expression. Genes at these loci are candidate regulators of increased expression of MIF after infection. Our study is the first data demonstrating that MIF expression is elevated in T. b. gambiense-infected human hosts but does not appear to contribute to pathology.

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Source
http://dx.doi.org/10.1016/j.meegid.2019.03.021DOI Listing

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