Assessment of the immunomodulatory effects of Luteolin on Chikungunya virus infection at the maternal-fetal interface in a murine model.

• Grant number: 25/07840-1
• Support Opportunities: Scholarships in Brazil - Master
• Start date: November 01, 2025
• End date: August 31, 2027
• Field of knowledge: Biological Sciences - Immunology - Applied Immunology
• Principal Investigator: Maria Notomi Sato
• Grantee: Rafaela Cassa Misaca
• Host Institution: Faculdade de Medicina (FM). Universidade de São Paulo (USP). São Paulo , SP, Brazil

Abstract

During pregnancy, the maternal immune system maintains a balance between tolerance to the fetus and vigilance against invading microorganisms. Some pathogens, such as the Chikungunya virus (CHIKV), can cause congenital infections, resulting in serious fetal alterations. Luteolin, a polyphenolic flavonoid found in various fruits and herbs, has anti-inflammatory, antiviral and neuroprotective properties.Given the lack of specific treatments and vaccines against CHIKV, investigating the modulatory effect of luteolin may represent an alternative to mitigate the impacts of congenital CHIKV infection. Therefore, we propose to develop a model of congenital CHIKV infection in mice to evaluate the immunological mechanisms of the maternal-fetal interface (MFI), such as the presence of IgG and IgA antibodies in serum and breast milk, the expression of antiviral, inflammatory and anti-inflammatory factors and the gene expression of receptors involved in the viral immune response (TLR3, TLR7/8, TLR9, MDA5, RIG-1) in the placenta. In addition, pregnant females will be treated with luteolin to assess viral load in serum, maternal and fetal tissue. In addition, the postnatal development of the offspring will be evaluated for survival and recovery over time and the cellular response in recovered animals will be determined by flow cytometry. Understanding the immunological mechanisms involved in MFI in CHIKV infection is essential to identify new interventions such as luteolin in modulating the inflammatory response and the outcome of CHIKV infection.