https://repositorio.ufu.br/handle/123456789/5162 2026-06-10T16:06:28Z 2026-06-10T16:06:28Z https://repositorio.ufu.br/handle/123456789/48739 2026-06-09T06:20:47Z 2026-05-29T00:00:00Z

Title: Memorial descritivo para promoção a classe de professor titular

2026-05-29T00:00:00Z https://repositorio.ufu.br/handle/123456789/48710 2026-05-22T06:21:53Z 2026-03-18T00:00:00Z

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 2026-05-16T06:23:36Z 2026-04-30T00:00:00Z

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 https://repositorio.ufu.br/handle/123456789/48636 2026-04-17T06:24:20Z 2026-03-10T00:00:00Z

Title: Uso dos genes Bmp4, Egr3 e Hsp70 como possíveis marcadores de toxicidade embrionária Abstract: Animal models remain relevant in scientific research because they allow the integrated investigation of physiological and pathological processes. Their use must be based on ethical and scientific criteria, considering the suitability of the model to the study objectives. Therefore, research should encourage the adoption of alternative methods, such as the use of embryos, which contribute to reducing the number of animals used, enable less invasive experimental approaches, and, whenever feasible, promote the partial or total replacement of animal use, in accordance with the principles of the 3 R’s (Reduction, Refinement, and Replacement). In this study, 33 Mus musculus embryos at the two-cell stage were exposed in vitro to the herbicides Pendimethalin and Prowl®H2O, with the aim of evaluating morphological alterations up to the blastocyst stage through in house and Gardner’s classification, based on the degree of blastocyst expansion and the quality of the inner cell mass (ICM) and the trophectoderm (TE), as well as changes in the expression of the genes Bmp4, Egr3, and Hsp70 using the RT-qPCR technique. Morphological analysis revealed developmental delay, cellular fragmentation, and cytoplasmic vacuolization, with more pronounced effects observed in the group exposed to Prowl®H2O. Molecular analysis demonstrated a significant increase in Bmp4 expression in the group treated with Prowl®H2O, while Egr3 and Hsp70 showed higher expression in embryos exposed to Pendimethalin, suggesting the activation of cellular stress pathways and dysregulation of developmental processes. These results indicate that both the isolated active ingredient and the commercial formulation can induce early morphological and molecular alterations, highlighting the importance of the integrated evaluation of morphological and molecular parameters in toxicity studies.

2026-03-10T00:00:00Z