Genetic variations of AIM2 and the inflammatory profile in latent tuberculosis infection: interfaces with latent toxoplasmosis and mental health

• Grant number: 26/01204-9
• Support Opportunities: Scholarships in Brazil - Scientific Initiation
• Start date: May 01, 2026
• End date: December 31, 2026
• Field of knowledge: Health Sciences - Medicine - Medical Clinics
• Principal Investigator: Eliana Peresi Lordelo
• Grantee: Julio Campos de Oliveira Júnior
• Host Institution: Faculdade de Ciências da Saúde (FCSA). Universidade do Oeste Paulista (UNOESTE). Presidente Prudente , SP, Brazil

Abstract

Tuberculosis (TB) remains one of the leading causes of global morbidity and mortality, and latent tuberculosis infection (LTBI) constitutes its main reservoir. The diagnostic methods currently in use, such as the tuberculin skin test (TST) and interferon-gamma release assays (IGRAs), have limitations in their ability to predict progression to active disease, highlighting the need for complementary biomarkers. In this context, the AIM2 (Absent in Melanoma 2) inflammasome stands out, as its activation results in the release of the cytokines IL-1¿ and IL-18, which are fundamental to the immune response against Mycobacterium tuberculosis (Mtb). The central focus of this project is to investigate the association between the rs1103577 and rs2276405 polymorphisms of the AIM2 gene and serum levels of IL-1¿ and IL-18 in individuals with LTBI, compared with individuals without latent infection. DNA and serum samples from an institutional biorepository will be analyzed, obtained from prison staff in Western São Paulo State, previously classified for LTBI by IGRA. Genotyping will be performed using real-time PCR (TaqMan), and cytokine levels will be measured by enzyme-linked immunosorbent assay (ELISA). Complementarily, within the scope of an expanded research project, interfaces with latent toxoplasmosis and psychosocial aspects will be explored, aiming to understand possible additional influences on the inflammatory profile. It is expected that the results will contribute to the understanding of immunogenetic mechanisms associated with LTBI and to the identification of relevant inflammatory biomarkers in vulnerable populations. (AU)