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MIF contributes to Trypanosoma brucei associated immunopathogenicity development

(2014) PLOS PATHOGENS. 10(9).
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Abstract
African trypanosomiasis is a chronic debilitating disease affecting the health and economic well-being of many people in developing countries. The pathogenicity associated with this disease involves a persistent inflammatory response, whereby M1-type myeloid cells, including Ly6C(high) inflammatory monocytes, are centrally implicated. A comparative gene analysis between trypanosusceptible and trypanotolerant animals identified MIF (macrophage migrating inhibitory factor) as an important pathogenic candidate molecule. Using MIF-deficient mice and anti-MIF antibody treated mice, we show that MIF mediates the pathogenic inflammatory immune response and increases the recruitment of inflammatory monocytes and neutrophils to contribute to liver injury in Trypanosoma brucei infected mice. Moreover, neutrophil-derived MIF contributed more significantly than monocyte-derived MIF to increased pathogenic liver TNF production and liver injury during trypanosome infection. MIF deficient animals also featured limited anemia, coinciding with increased iron bio-availability, improved erythropoiesis and reduced RBC clearance during the chronic phase of infection. Our data suggest that MIF promotes the most prominent pathological features of experimental trypanosome infections (i.e. anemia and liver injury), and prompt considering MIF as a novel target for treatment of trypanosomiasis-associated immunopathogenicity.
Keywords
AFRICAN TRYPANOSOMIASIS, MIGRATION INHIBITORY FACTOR, MACROPHAGE ACTIVATION, ANEMIA, ERYTHROPOIESIS, INFLAMMATION, INFECTION, GENE, MICE, TRYPANOTOLERANCE

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MLA
Stijlemans, Benoit et al. “MIF Contributes to Trypanosoma Brucei Associated Immunopathogenicity Development.” PLOS PATHOGENS 10.9 (2014): n. pag. Print.
APA
Stijlemans, Benoit, Leng, L., Brys, L., Sparkes, A., Vansintjan, L., Caljon, G., Raes, G., et al. (2014). MIF contributes to Trypanosoma brucei associated immunopathogenicity development. PLOS PATHOGENS, 10(9).
Chicago author-date
Stijlemans, Benoit, Lin Leng, Lea Brys, Amanda Sparkes, Liese Vansintjan, Guy Caljon, Geert Raes, et al. 2014. “MIF Contributes to Trypanosoma Brucei Associated Immunopathogenicity Development.” Plos Pathogens 10 (9).
Chicago author-date (all authors)
Stijlemans, Benoit, Lin Leng, Lea Brys, Amanda Sparkes, Liese Vansintjan, Guy Caljon, Geert Raes, Jan Van Den Abbeele, Jo A Van Ginderachter, Alain Beschin, Richard Bucala, and Patrick De Baetselier. 2014. “MIF Contributes to Trypanosoma Brucei Associated Immunopathogenicity Development.” Plos Pathogens 10 (9).
Vancouver
1.
Stijlemans B, Leng L, Brys L, Sparkes A, Vansintjan L, Caljon G, et al. MIF contributes to Trypanosoma brucei associated immunopathogenicity development. PLOS PATHOGENS. 2014;10(9).
IEEE
[1]
B. Stijlemans et al., “MIF contributes to Trypanosoma brucei associated immunopathogenicity development,” PLOS PATHOGENS, vol. 10, no. 9, 2014.
@article{6905586,
  abstract     = {{African trypanosomiasis is a chronic debilitating disease affecting the health and economic well-being of many people in developing countries. The pathogenicity associated with this disease involves a persistent inflammatory response, whereby M1-type myeloid cells, including Ly6C(high) inflammatory monocytes, are centrally implicated. A comparative gene analysis between trypanosusceptible and trypanotolerant animals identified MIF (macrophage migrating inhibitory factor) as an important pathogenic candidate molecule. Using MIF-deficient mice and anti-MIF antibody treated mice, we show that MIF mediates the pathogenic inflammatory immune response and increases the recruitment of inflammatory monocytes and neutrophils to contribute to liver injury in Trypanosoma brucei infected mice. Moreover, neutrophil-derived MIF contributed more significantly than monocyte-derived MIF to increased pathogenic liver TNF production and liver injury during trypanosome infection. MIF deficient animals also featured limited anemia, coinciding with increased iron bio-availability, improved erythropoiesis and reduced RBC clearance during the chronic phase of infection. Our data suggest that MIF promotes the most prominent pathological features of experimental trypanosome infections (i.e. anemia and liver injury), and prompt considering MIF as a novel target for treatment of trypanosomiasis-associated immunopathogenicity.}},
  articleno    = {{e1004414}},
  author       = {{Stijlemans, Benoit and Leng, Lin and Brys, Lea and Sparkes, Amanda and Vansintjan, Liese and Caljon, Guy and Raes, Geert and Van Den Abbeele, Jan and Van Ginderachter, Jo A and Beschin, Alain and Bucala, Richard and De Baetselier, Patrick}},
  issn         = {{1553-7366}},
  journal      = {{PLOS PATHOGENS}},
  keywords     = {{AFRICAN TRYPANOSOMIASIS,MIGRATION INHIBITORY FACTOR,MACROPHAGE ACTIVATION,ANEMIA,ERYTHROPOIESIS,INFLAMMATION,INFECTION,GENE,MICE,TRYPANOTOLERANCE}},
  language     = {{eng}},
  number       = {{9}},
  pages        = {{13}},
  title        = {{MIF contributes to Trypanosoma brucei associated immunopathogenicity development}},
  url          = {{http://dx.doi.org/10.1371/journal.ppat.1004414}},
  volume       = {{10}},
  year         = {{2014}},
}

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