CHARACTERIZATION OF MICROGLIA AND EDGE-ASSOCIATED MACROPHAGES INDUCED BY MEDIATORS DERIVED FROM ALLERGIC LUNG INFLAMMATION

• Grant number: 23/18185-9
• Support Opportunities: Scholarships in Brazil - Scientific Initiation
• Start date: April 01, 2024
• End date: December 31, 2024
• Field of knowledge: Biological Sciences - Immunology
• Principal Investigator: Vânia Luiza Deperon Bonato
• Grantee: Gabriela Maria da Costa Ferreira
• Host Institution: Faculdade de Medicina de Ribeirão Preto (FMRP). Universidade de São Paulo (USP). Ribeirão Preto , SP, Brazil

Abstract

The asthma is a chronic disease of the world reach, causing inflammation and remodeling in the lung tissue. Recent studies suggest what the inflammation causing of the asthma has systemic effect, affecting the central neurvous system (CNS). The inflammation response in the lung of patient with allergic asthma or Th2 high is characterized by the presence of IL-4, IL-5, IL-13. This cytokines can circulate systemic and reach the CNS, developing neuroinflammation. The microglia, resident macrophages of the CNS, when exposed to inflammatory mediator can become dysfunctional, induced death of neurons and contributes to developing a diseases neurodegeneration and mental disorders, with anxiety and depression. The objective of this project is to evaluate activation of microglia and macrophages associated with edge for inflammatory mediator coming serum from the mouse subject to an experimental model of the asthma. Our hypotysis is throung contact with circulating inflammator mediator coming the lung inflammation, this resident cells in CNS can activated in such a way inducing neuronal death. For the test hypothesis, are deliniation this is expertimental: evalue activation microglias and macrophages associated with egde for contact with serum from the mouse subject to an experimental model of the asthma, and evalue neural viability, caused for activation of the microglias and macrophages associated with edge has prior contact with serum from the mouse subject to an experimental model of the asthma. Thrus, we seek best understands the interaction in the axle lung inflammation on asthm and CNS, with purpose the big investigation this a systemic inflammation can contribute to mental disorder