| Grant number: | 24/10025-5 |
| Support Opportunities: | Scholarships in Brazil - Scientific Initiation |
| Start date: | August 01, 2024 |
| End date: | July 31, 2025 |
| Field of knowledge: | Biological Sciences - Microbiology - Applied Microbiology |
| Principal Investigator: | Karen Spadari Ferreira |
| Grantee: | Gabrielly Torres dos Santos |
| Host Institution: | Instituto de Ciências Ambientais, Químicas e Farmacêuticas (ICAQF). Universidade Federal de São Paulo (UNIFESP). Campus Diadema. Diadema , SP, Brazil |
Abstract The Sporothrix brasiliensis fungus is one of the main species that causes zoonotic sporotrichosis. This disease has seen a growing number of cases in Brazil, especially in the Southeast, making it an endemic zoonosis that affects public health and lacks the means to contain and treat it. In this scenario, it has been observed that Sporothrix spp. fungi are thermodimorphic and can cause subcutaneous and systemic mycoses in more severe cases, in a way that the immune response and the association of fungal and immune response macrophages EVs are related to the pathogen-host interaction. Therefore, it is known that the Extracellular Vesicles (EVs) of pathogenic yeasts have extremely important molecules in the harmful agent's escape mechanism against the immune response, as well it is known that the EVs produced by host macrophages may have the capacity to act in the fungal growth inhibition due to the production of cytokines and surface molecules. However, the method of action of the vesicles produced by pre-activated macrophages by contact with the fungus is not yet fully understood, so their role in inducing the immune response must be analyzed in order to understand their action. Thus, this research seeks to assimilate and understand the mechanism of action of macrophage extracellular vesicles and the feasibility of associating them with antifungal drugs already used in the treatment of sporotrichosis, such as itraconazole, in order to analyze new methods of combating Sporothrix brasiliensis in J774 cell strains infected with pathogen's conidia. | |
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