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Transcriptomic analysis reveals that mTOR pathway can be modulated in macrophage cells by the presence of cryptococcal cells

Cryptococcus neoformans and Cryptococcus gattii are the etiological agents of cryptococcosis, a high mortality disease. The development of such disease depends on the interaction of fungal cells with macrophages, in which they can reside and replicate. In order to dissect the molecular mechanisms by...

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Detalles Bibliográficos
Autores principales: Piffer, Alícia C., dos Santos, Francine M., Thomé, Marcos P., Diehl, Camila, Garcia, Ane Wichine Acosta, Kinskovski, Uriel Perin, Schneider, Rafael de Oliveira, Gerber, Alexandra, Feltes, Bruno César, Schrank, Augusto, Vasconcelos, Ana Tereza R., Lenz, Guido, Kmetzsch, Lívia, Vainstein, Marilene H., Staats, Charley C.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Sociedade Brasileira de Genética 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8341293/
https://www.ncbi.nlm.nih.gov/pubmed/34352067
http://dx.doi.org/10.1590/1678-4685-GMB-2020-0390
Descripción
Sumario:Cryptococcus neoformans and Cryptococcus gattii are the etiological agents of cryptococcosis, a high mortality disease. The development of such disease depends on the interaction of fungal cells with macrophages, in which they can reside and replicate. In order to dissect the molecular mechanisms by which cryptococcal cells modulate the activity of macrophages, a genome-scale comparative analysis of transcriptional changes in macrophages exposed to Cryptococcus spp. was conducted. Altered expression of nearly 40 genes was detected in macrophages exposed to cryptococcal cells. The major processes were associated with the mTOR pathway, whose associated genes exhibited decreased expression in macrophages incubated with cryptococcal cells. Phosphorylation of p70S6K and GSK-3β was also decreased in macrophages incubated with fungal cells. In this way, Cryptococci presence could drive the modulation of mTOR pathway in macrophages possibly to increase the survival of the pathogen.