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 Toxoplasma gondii. As the MIF function in congenital toxoplasmosis is not fully elucidat...
| Main Authors: | , , , , , , , , , , , , , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Frontiers Media S.A.
2018-05-01
|
| Series: | Frontiers in Microbiology |
| Subjects: | |
| Online Access: | http://journal.frontiersin.org/article/10.3389/fmicb.2018.00906/full |
| id |
doaj-da0c446364e3411cb01151cef8779651 |
|---|---|
| record_format |
Article |
| collection |
DOAJ |
| language |
English |
| format |
Article |
| sources |
DOAJ |
| author |
Angelica O. Gomes Bellisa F. Barbosa Priscila S. Franco Mayara Ribeiro Rafaela J. Silva Paula S. G. Gois Karine C. Almeida Mariana B. Angeloni Andressa S. Castro Pâmela M. Guirelli João V. Cândido Javier E. L. Chica Neide M. Silva Tiago W. P. Mineo José R. Mineo Eloisa A. V. Ferro |
| spellingShingle |
Angelica O. Gomes Bellisa F. Barbosa Priscila S. Franco Mayara Ribeiro Rafaela J. Silva Paula S. G. Gois Karine C. Almeida Mariana B. Angeloni Andressa S. Castro Pâmela M. Guirelli João V. Cândido Javier E. L. Chica Neide M. Silva Tiago W. P. Mineo José R. Mineo Eloisa A. V. Ferro Macrophage Migration Inhibitory Factor (MIF) Prevents Maternal Death, but Contributes to Poor Fetal Outcome During Congenital Toxoplasmosis Frontiers in Microbiology Toxoplasma gondii maternal-fetal interface MIF CD74 IDO immune response |
| author_facet |
Angelica O. Gomes Bellisa F. Barbosa Priscila S. Franco Mayara Ribeiro Rafaela J. Silva Paula S. G. Gois Karine C. Almeida Mariana B. Angeloni Andressa S. Castro Pâmela M. Guirelli João V. Cândido Javier E. L. Chica Neide M. Silva Tiago W. P. Mineo José R. Mineo Eloisa A. V. Ferro |
| author_sort |
Angelica O. Gomes |
| title |
Macrophage Migration Inhibitory Factor (MIF) Prevents Maternal Death, but Contributes to Poor Fetal Outcome During Congenital Toxoplasmosis |
| title_short |
Macrophage Migration Inhibitory Factor (MIF) Prevents Maternal Death, but Contributes to Poor Fetal Outcome During Congenital Toxoplasmosis |
| title_full |
Macrophage Migration Inhibitory Factor (MIF) Prevents Maternal Death, but Contributes to Poor Fetal Outcome During Congenital Toxoplasmosis |
| title_fullStr |
Macrophage Migration Inhibitory Factor (MIF) Prevents Maternal Death, but Contributes to Poor Fetal Outcome During Congenital Toxoplasmosis |
| title_full_unstemmed |
Macrophage Migration Inhibitory Factor (MIF) Prevents Maternal Death, but Contributes to Poor Fetal Outcome During Congenital Toxoplasmosis |
| title_sort |
macrophage migration inhibitory factor (mif) prevents maternal death, but contributes to poor fetal outcome during congenital toxoplasmosis |
| publisher |
Frontiers Media S.A. |
| series |
Frontiers in Microbiology |
| issn |
1664-302X |
| publishDate |
2018-05-01 |
| description |
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 Toxoplasma gondii. As the MIF function in congenital toxoplasmosis is not fully elucidated yet, the present study brings new insights for T. gondii 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 T. gondii (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 T. gondii infection, favors fetal damage. |
| topic |
Toxoplasma gondii maternal-fetal interface MIF CD74 IDO immune response |
| url |
http://journal.frontiersin.org/article/10.3389/fmicb.2018.00906/full |
| work_keys_str_mv |
AT angelicaogomes macrophagemigrationinhibitoryfactormifpreventsmaternaldeathbutcontributestopoorfetaloutcomeduringcongenitaltoxoplasmosis AT bellisafbarbosa macrophagemigrationinhibitoryfactormifpreventsmaternaldeathbutcontributestopoorfetaloutcomeduringcongenitaltoxoplasmosis AT priscilasfranco macrophagemigrationinhibitoryfactormifpreventsmaternaldeathbutcontributestopoorfetaloutcomeduringcongenitaltoxoplasmosis AT mayararibeiro macrophagemigrationinhibitoryfactormifpreventsmaternaldeathbutcontributestopoorfetaloutcomeduringcongenitaltoxoplasmosis AT rafaelajsilva macrophagemigrationinhibitoryfactormifpreventsmaternaldeathbutcontributestopoorfetaloutcomeduringcongenitaltoxoplasmosis AT paulasggois macrophagemigrationinhibitoryfactormifpreventsmaternaldeathbutcontributestopoorfetaloutcomeduringcongenitaltoxoplasmosis AT karinecalmeida macrophagemigrationinhibitoryfactormifpreventsmaternaldeathbutcontributestopoorfetaloutcomeduringcongenitaltoxoplasmosis AT marianabangeloni macrophagemigrationinhibitoryfactormifpreventsmaternaldeathbutcontributestopoorfetaloutcomeduringcongenitaltoxoplasmosis AT andressascastro macrophagemigrationinhibitoryfactormifpreventsmaternaldeathbutcontributestopoorfetaloutcomeduringcongenitaltoxoplasmosis AT pamelamguirelli macrophagemigrationinhibitoryfactormifpreventsmaternaldeathbutcontributestopoorfetaloutcomeduringcongenitaltoxoplasmosis AT joaovcandido macrophagemigrationinhibitoryfactormifpreventsmaternaldeathbutcontributestopoorfetaloutcomeduringcongenitaltoxoplasmosis AT javierelchica macrophagemigrationinhibitoryfactormifpreventsmaternaldeathbutcontributestopoorfetaloutcomeduringcongenitaltoxoplasmosis AT neidemsilva macrophagemigrationinhibitoryfactormifpreventsmaternaldeathbutcontributestopoorfetaloutcomeduringcongenitaltoxoplasmosis AT tiagowpmineo macrophagemigrationinhibitoryfactormifpreventsmaternaldeathbutcontributestopoorfetaloutcomeduringcongenitaltoxoplasmosis AT josermineo macrophagemigrationinhibitoryfactormifpreventsmaternaldeathbutcontributestopoorfetaloutcomeduringcongenitaltoxoplasmosis AT eloisaavferro macrophagemigrationinhibitoryfactormifpreventsmaternaldeathbutcontributestopoorfetaloutcomeduringcongenitaltoxoplasmosis |
| _version_ |
1725434285562789888 |
| spelling |
doaj-da0c446364e3411cb01151cef87796512020-11-25T00:03:23ZengFrontiers Media S.A.Frontiers in Microbiology1664-302X2018-05-01910.3389/fmicb.2018.00906350719Macrophage Migration Inhibitory Factor (MIF) Prevents Maternal Death, but Contributes to Poor Fetal Outcome During Congenital ToxoplasmosisAngelica O. Gomes0Bellisa F. Barbosa1Priscila S. Franco2Mayara Ribeiro3Rafaela J. Silva4Paula S. G. Gois5Karine C. Almeida6Mariana B. Angeloni7Andressa S. Castro8Pâmela M. Guirelli9João V. Cândido10Javier E. L. Chica11Neide M. Silva12Tiago W. P. Mineo13José R. Mineo14Eloisa A. V. Ferro15Institute of Natural and Biological Sciences, Federal University of Triângulo Mineiro, Uberaba, BrazilLaboratory of Immunophysiology of Reproduction, Institute of Biomedical Science, Federal University of Uberlândia, Uberlândia, BrazilLaboratory of Immunophysiology of Reproduction, Institute of Biomedical Science, Federal University of Uberlândia, Uberlândia, BrazilLaboratory of Immunophysiology of Reproduction, Institute of Biomedical Science, Federal University of Uberlândia, Uberlândia, BrazilLaboratory of Immunophysiology of Reproduction, Institute of Biomedical Science, Federal University of Uberlândia, Uberlândia, BrazilLaboratory of Immunophysiology of Reproduction, Institute of Biomedical Science, Federal University of Uberlândia, Uberlândia, BrazilLaboratory of Immunophysiology of Reproduction, Institute of Biomedical Science, Federal University of Uberlândia, Uberlândia, BrazilLaboratory of Immunophysiology of Reproduction, Institute of Biomedical Science, Federal University of Uberlândia, Uberlândia, BrazilLaboratory of Immunophysiology of Reproduction, Institute of Biomedical Science, Federal University of Uberlândia, Uberlândia, BrazilLaboratory of Immunophysiology of Reproduction, Institute of Biomedical Science, Federal University of Uberlândia, Uberlândia, BrazilInstitute of Natural and Biological Sciences, Federal University of Triângulo Mineiro, Uberaba, BrazilInstitute of Natural and Biological Sciences, Federal University of Triângulo Mineiro, Uberaba, BrazilLaboratory of Immunopathology, Institute of Biomedical Sciences, Federal University of Uberlândia, Uberlândia, BrazilLaboratory of Immunoparasitology, Institute of Biomedical Science, Federal University of Uberlândia, Uberlândia, BrazilLaboratory of Immunoparasitology, Institute of Biomedical Science, Federal University of Uberlândia, Uberlândia, BrazilLaboratory of Immunophysiology of Reproduction, Institute of Biomedical Science, Federal University of Uberlândia, Uberlândia, BrazilMigration 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 Toxoplasma gondii. As the MIF function in congenital toxoplasmosis is not fully elucidated yet, the present study brings new insights for T. gondii 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 T. gondii (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 T. gondii infection, favors fetal damage.http://journal.frontiersin.org/article/10.3389/fmicb.2018.00906/fullToxoplasma gondiimaternal-fetal interfaceMIFCD74IDOimmune response |