https://repositorio.ufu.br/handle/123456789/5162 2026-07-03T15:28:40Z https://repositorio.ufu.br/handle/123456789/48748 Title: Memorial acadêmico 2026-05-29T00:00:00Z https://repositorio.ufu.br/handle/123456789/48739 Title: Memorial descritivo para promoção a classe de professor titular 2026-05-29T00:00:00Z https://repositorio.ufu.br/handle/123456789/48710 Title: O papel da NINJ1 na resposta inflamatória mediada por piroptose em Toxoplasma gondii e Neospora caninum Abstract: The innate immune system is crucial for defending against intracellular pathogens, such as Apicomplexan parasites, including Toxoplasma gondii and Neospora caninum. Programmed cell death (PCD) pathways, like pyroptosis, play a key role in limiting parasite replication and promoting inflammatory responses. Pyroptosis is characterized by inflammasome activation and gasdermin pore formation, leading to plasma membrane permeabilization. Recently, Nerve Injury-Induced Protein 1 (NINJ1) has been identified as a key mediator of terminal membrane rupture during inflammatory cell death. However, its role during Apicomplexan infections remains poorly understood. To address this, the study first conducted a review of PCD pathways in Apicomplexan parasites to identify existing knowledge gaps. It then investigated the role of NINJ1 in T. gondii and N. caninum infections. NINJ1-deficient DC2.4 cells (ΔNinj1) were generated using CRISPR-Cas9, and functional assays were performed to assess membrane permeabilization, cell lysis (via PI uptake and LDH release), and caspase-1/11 activation. Additionally, bone marrow-derived macrophages (BMDMs) from wild-type and caspase-1/11-deficient mice were used to assess inflammasome-dependent membrane permeability. Intracellular parasite burden was analyzed in DC2.4 cells and RAW 2.6.4.2 macrophages, comparing parasite replication in normal and NINJ1-deficient cells. The results showed that NINJ1 expression increases during infection and that its absence enhances parasite replication while significantly reducing cell lysis. Loss of NINJ1 did not affect caspase-1/11 activation or initial membrane permeabilization, but LDH release was greatly reduced, indicating that NINJ1 is essential for the terminal phase of plasma membrane rupture. These findings position NINJ1 as a critical effector linking inflammasome activation to terminal cellular disintegration during Apicomplexan infections. 2026-03-18T00:00:00Z https://repositorio.ufu.br/handle/123456789/48698 Title: Reatividade sorológica anti-toxocara em doenças reumáticas autoimunes revela supressão seletiva de IgG4 no lúpus eritematoso sistêmico Abstract: Helminth exposure has been suggested as a modulating factor in autoimmune inflammation; however, gaps remain regarding the quality of anti-helminth immune responses in autoimmune rheumatic diseases. In this study, we analyzed anti-Toxocara canis seroreactivity profiles in individuals with rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), and spondyloarthritis (SpA), compared with controls, and also investigated potential clinical associations. A cross-sectional case-control study was conducted, including 442 participants. Initially, samples were tested for anti -T. canis IgG using native TES antigen, and reactive samples were subsequently evaluated using the recombinant chimeric antigen rSHORT for the detection of total IgG, IgG1, and IgG4. Disease activity was assessed using SLEDAI in SLE, and functional disability using HAQ-DI. The results demonstrated a high frequency of anti-T. canis seroreactivity in the studied population. After adjustment for demographic variables, patients with SLE showed higher odds of total IgG positivity compared with controls, whereas IgG4 seroreactivity was significantly reduced. No independent associations were observed between IgG isotypes and HAQ-DI in patients with RA or SpA. Within the SLE group, higher eosinophil levels were independently associated with lower disease activity. Overall, these findings indicate heterogeneous patterns of anti-Toxocara serological responses in autoimmune rheumatic diseases, with SLE showing the most distinctive profile, characterized by preserved total IgG responses alongside reduced IgG4 seroreactivity. Furthermore, eosinophils, rather than IgG4, were more strongly associated with lower disease activity in SLE. 2026-04-30T00:00:00Z