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MIF contributes to Trypanosoma brucei associated immunopathogenicity development

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dc.contributor.author Stijlemans, B.
dc.contributor.author Leng, L.
dc.contributor.author Brys, L.
dc.contributor.author Sparkes, A.
dc.contributor.author Vansintjan, L.
dc.contributor.author Caljon, G.
dc.contributor.author Raes, G.
dc.contributor.author Van Den Abbeele, J.
dc.contributor.author Van Ginderachter, J. A.
dc.contributor.author Beschin, A.
dc.contributor.author Bucala, R.
dc.contributor.author De Baetselier, P.
dc.date.accessioned 2015-02-24T16:02:28Z
dc.date.available 2015-02-24T16:02:28Z
dc.date.issued 2014
dc.identifier.issn 1553-7366
dc.identifier.doi http://dx.doi.org/10.1371/journal.ppat.1004414
dc.identifier.other ITG-B6B
dc.identifier.other ITG-B8A
dc.identifier.other DBM
dc.identifier.other U-VPROT
dc.identifier.other JIF
dc.identifier.other DOI
dc.identifier.other OAJ
dc.identifier.other E-only
dc.identifier.other FTA
dc.identifier.other Abstract
dc.identifier.other UPD57
dc.identifier.uri http://hdl.handle.net/10390/8288
dc.description.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. en_US
dc.language English en_US
dc.subject Protozoal diseases en_US
dc.subject Sleeping sickness en_US
dc.subject Trypanosomiasis, African en_US
dc.subject Trypanosoma brucei en_US
dc.subject Vectors en_US
dc.subject Tsetse flies en_US
dc.subject Glossina morsitans morsitans en_US
dc.subject Pathogenicity en_US
dc.subject Gene sequencing en_US
dc.subject Macrophage activation en_US
dc.subject Inflammatory reactions en_US
dc.subject Monocytes en_US
dc.subject Neutrophil en_US
dc.subject Liver en_US
dc.subject Anemia en_US
dc.subject Targets en_US
dc.title MIF contributes to Trypanosoma brucei associated immunopathogenicity development en_US
dc.type Article-E en_US
dc.citation.issue 9 en_US
dc.citation.jtitle PLoS Pathogens en_US
dc.citation.volume 10 en_US
dc.citation.pages e1004414 en_US
dc.identifier.pmid http://www.ncbi.nlm.nih.gov/pubmed/25255103
dc.citation.jabbreviation PLoS Pathog en_US


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