Macrophage Migration Inhibitory Factor (MIF) Prevents Maternal Death, but Contributes to Poor Fetal Outcome During Congenital Toxoplasmosis

Migration inhibitory factor (MIF) is a pro-inflammatory cytokine that plays important roles in physiology, pathology, immunology and parasitology, including the control of infection by protozoa parasites such as . As the MIF function in congenital toxoplasmosis is not fully elucidated yet, the prese...

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Published in:	Frontiers in microbiology Vol. 9; p. 906
Main Authors:	Gomes, Angelica O, Barbosa, Bellisa F, Franco, Priscila S, Ribeiro, Mayara, Silva, Rafaela J, Gois, Paula S G, Almeida, Karine C, Angeloni, Mariana B, Castro, Andressa S, Guirelli, Pâmela M, Cândido, João V, Chica, Javier E L, Silva, Neide M, Mineo, Tiago W P, Mineo, José R, Ferro, Eloisa A V
Format:	Journal Article
Language:	English
Published:	Switzerland Frontiers Media S.A 08-05-2018
Subjects:	CD74 IDO immune response maternal-fetal interface Microbiology MIF Toxoplasma gondii CD74 Toxoplasma gondii MIF maternal-fetal interface IDO immune response
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Summary:	Migration inhibitory factor (MIF) is a pro-inflammatory cytokine that plays important roles in physiology, pathology, immunology and parasitology, including the control of infection by protozoa parasites such as . As the MIF function in congenital toxoplasmosis is not fully elucidated yet, the present study brings new insights for infection in the absence of MIF based on pregnant C57BL/6MIF mouse models. Pregnant C57BL/6MIF and C57BL/6WT mice were infected with 05 cysts of (ME49 strain) on the first day of pregnancy (dop) and were euthanized at 8 dop. Non-pregnant and non-infected females were used as control. Our results demonstrated that MIF mice have more accentuated change in body weight and succumbed to infection first than their WT counterparts. Otherwise, pregnancy outcome was less destructive in MIF mice compared to WT ones, and the former had an increase in the mast cell recruitment and IDO expression and consequently presented less inflammatory cytokine production. Also, MIF receptor (CD74) was upregulated in MIF mice, indicating that a compensatory mechanism may be required in this model of study. The global absence of MIF was associated with attenuation of pathology in congenital toxoplasmosis, but resulted in female death probably because of uncontrolled infection. Altogether, ours results demonstrated that part of the immune response that protects a pregnant female from infection, favors fetal damage.
Bibliography:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Edited by: Alain Pierre Gobert, Vanderbilt University Medical Center, United States Reviewed by: Emma Harriet Wilson, University of California, Riverside, United States; Xiangrui Li, Nanjing Agricultural University, China This article was submitted to Infectious Diseases, a section of the journal Frontiers in Microbiology
ISSN:	1664-302X 1664-302X
DOI:	10.3389/fmicb.2018.00906