| Autor: |
Pires, Luiza B., Peixoto-Rodrigues, Maria C., Eloi, Jéssica F., Cascabulho, Cynthia M., Barbosa, Helene S., Santiago, Marcelo F., Adesse, Daniel |
| Zdroj: |
American Journal of Pathology; July 2023, Vol. 193 Issue: 7 p977-994, 18p |
| Abstrakt: |
Congenital toxoplasmosis constitutes a major cause of pre- and postnatal complications. Fetal infection with Toxoplasma gondiiinfluences development and can lead to microcephaly, encephalitis, and neurologic abnormalities. Systematic studies concerning the effects of neural progenitor cell infection with T. gondiiare unavailable. Cortical intermediate progenitor cells cultivated as neurospheres obtained from E16.5 Swiss Webster mice were infected with T. gondii(ME49 strain) tachyzoites to mimic the developing mouse cerebral cortex in vitro. Infection was associated with decreased cell proliferation, detected by Ki-67 staining at 48 and 72 hours after infection in floating neurospheres, and reduced cellularity at 96 hours. Transient decreases in the expression of the neurogenesis-related transcription factors T-box brain protein 1, mouse atonal homolog protein 1, and hairy and enhancer of split protein 1 were found in infected cultures, while the level of transcription factor SOX-2 remained unaltered. Neurogenic potential, assessed in plated neurospheres, was impaired in infected cultures, as indicated by decreased late neuronal marker neurofilament heavy chain immunoreactivity. Infected cultures exhibited decreased overall migration rates at 48 and 120 hours. These findings indicate that T. gondiiinfection of neural progenitor cells may lead to reduced neurogenesis due to an imbalance in cell proliferation alongside an altered migratory profile. If translated to the in vivosituation, these data could explain, in part, cortical malformations in congenitally infected individuals. |
| Databáze: |
Supplemental Index |
| Externí odkaz: |
|
