Trypanosoma evansi impacts on embryonic neural progenitor cell functions

Autor(es):Mostrar menos -

Fracasso, Mateus ^[1] ; Pillat, Micheli M. ^[2] ; Bottari, Nathieli B. ^[1] ; da Silva, Anielen D. ^[1] ; Grando, Thirssa H. ^[3] ; Matos, Antonio F. I. M. ^[3] ; Petry, Leticia S. ^[3] ; Ulrich, Henning ^[2] ; de Andrade, Cinthia M. ^{[1, 3]} ; Monteiro, Silvia G. ^[3] ; Da Silva, Aleksandro S. ^[4]

Afiliação do(s) autor(es)

^[1] Univ Fed Santa Maria, Dept Biochem & Mol Biol, Grad Program Toxicol Biochem, Santa Maria, RS - Brazil

^[2] Univ Sao Paulo, Inst Chem, Dept Biochem, Sao Paulo, SP - Brazil

^[3] Univ Fed Santa Maria, Dept Parasitol Microbiol & Immunol, Grad Program Vet Med, Santa Maria, RS - Brazil

^[4] Univ Estado Santa Catarina UDESC, Grad Program Anim Sci, Chapeco, SC - Brazil

• Tipo de documento: Artigo Científico
• Fonte: Microbial Pathogenesis; v. 136, NOV 2019.
• Citações Web of Science: 0

Resumo

Trypanosoma evansi appears to have a significant tropism for brain tissue in its chronic and acute phases. The most common symptoms of this brain infection are motor incoordination, meningoencephalitis, demyelination, and anemia. There have only been few studies of the effects of T. evansi infection on neuronal differentiation and brain plasticity. Here, we investigated the impact of the congenital T. evansi infection on brain development in mice. We collected telencephalon-derived neural progenitor cells (NPCs) from T. evansi uninfected and infected mice, and cultivated them into neurospheres. We found that T. evansi significantly decreased the number of cells during development of neurospheres. Analysis of neurosphere differentiation revealed that T. evansi infection significantly increased neural migration. We also observed that T. evansi promoted expression of glial fibrillary acidic protein (GFAP) in infected cells. These data suggest that congenital T. evansi infection may affect embryonic brain development. (AU)

• Processo FAPESP: 12/50880-4 - Células-tronco: dos papéis de receptores de cininas e purinas às aplicações terapêuticas
• Beneficiário: Alexander Henning Ulrich
• Modalidade de apoio: Auxílio à Pesquisa - Temático