Zika virus infection of first trimester trophoblast cells affects cell migration, metabolism and immune homeostasis control
Autor: | Guillermina Calo, Claudia Perez Leiros, Daiana Vota, Daniel Paparini, Federico Giovannoni, Rosanna Ramhorst, Cybele C. García, Vanesa Hauk, Maria Florencia Torti, Fátima Merech |
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Rok vydání: | 2020 |
Předmět: |
CD4-Positive T-Lymphocytes
0301 basic medicine Physiology Placenta CD14 Clinical Biochemistry Population Biology Congenital Abnormalities 03 medical and health sciences Fetus 0302 clinical medicine Immune system Cell Movement Pregnancy medicine Humans education Cells Cultured education.field_of_study Glucose Transporter Type 3 Zika Virus Infection Brain-Derived Neurotrophic Factor Trophoblast FOXP3 Placentation Cell migration Zika Virus Cell Biology Virology Trophoblasts Pregnancy Trimester First Glucose 030104 developmental biology medicine.anatomical_structure 030220 oncology & carcinogenesis Viperin embryonic structures Female Energy Metabolism Vasoactive Intestinal Peptide |
Zdroj: | Journal of Cellular Physiology. 236:4913-4925 |
ISSN: | 1097-4652 0021-9541 |
Popis: | Zika virus (ZIKV) re-emerged after circulating almost undetected for many years and the last spread in 2015 was the major outbreak reported. ZIKV infection was associated with congenital fetal growth anomalies such as microcephaly, brain calcifications, and low birth weight related to fetal growth restriction. In this study, we investigated the effect of ZIKV infection on first trimester trophoblast cell function and metabolism. We also studied the interaction of trophoblast cells with decidual immune populations. Results presented here demonstrate that ZIKV infection triggered a strong antiviral response in first trimester cytotrophoblast-derived cells, impaired cell migration, increased glucose uptake and GLUT3 expression, and reduced brain derived neurotrophic factor (BDNF) expression. ZIKV infection also conditioned trophoblast cells to favor a tolerogenic response since an increased recruitment of CD14+ monocytes bearing an anti-inflammatory profile, increased CD4+ T cells and NK CD56Dim and NK CD56Bright populations and an increment in the population CD4+ FOXP3+ IL-10+ cells was observed. Interestingly, when ZIKV infection of trophoblast cells occurred in the presence of the vasoactive intestinal peptide (VIP) there was lower detection of viral RNA and reduced toll-like receptor-3 and viperin messenger RNA expression, along with reduced CD56Dim cells trafficking to trophoblast conditioned media. The effects of ZIKV infection on trophoblast cell function and immune-trophoblast interaction shown here could contribute to defective placentation and ZIKV persistence at the fetal-maternal interface. The inhibitory effect of VIP on ZIKV infection of trophoblast cells highlights its potential as a candidate molecule to interfere ZIKV infection during early pregnancy. |
Databáze: | OpenAIRE |
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