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Ceron, J. J.

Publications and source records attributed to Ceron, J. J..

2 recordsLinked to original sources

Prediction of early Toxoplasma gondii infection during pregnancy combining host biomarkers and machine learning

Toxoplasma gondii is a major cause of reproductive failure and severe gestational complications in both humans and small ruminants and early diagnosis is essential to prevent adverse outcomes. In sheep, congenital toxoplasmosis can trigger early fetal death (EFD) during the acute phase of the infection (days 7-14 post-infection) when conventional diagnosis methods are ineffective. Therefore, this study aimed to identify early infection biomarkers using a machine learning approach to support EFD diagnosis and providing a translational foundation for early diagnostic strategies in human toxoplasmosis. For that, 27 serum biomarkers (cytokines, acute-phase proteins, oxidative stress and hemostatic parameters) were evaluated during the early stage of infection in 22 pregnant sheep experimentally challenged with T. gondii and 6 uninfected controls. To assess diagnostic specificity, models were tested using sera from animals experimentally infected with other abortifacient agents (Neospora caninum and Chlamydia abortus) and validated with samples from 19 natural abortion outbreaks. A four-biomarkers panel, encompassing CXCL9, CXCL10, IFN-{gamma}, and serum amyloid A, achieved over 74% accuracy in the specific detection of early T. gondii infection and 100% of sensitivity when studying natural infection cases. This approach might support the development of rapid diagnostic strategies, improving early intervention and disease management in livestock production systems. Its translation to human medicine could also aid in addressing current diagnostic gaps and facilitate timely interventions to prevent congenital toxoplasmosis and pregnancy loss in women.

immunology↗

ND-13, a DJ-1 derived peptide, as a novel pharmacological approach in the prevention of NLRP3 inflammasome activity in Diabetic Nephropathy

Diabetic nephropathy is the most important cause of renal failure worldwide and is characterized by sustained inflammation regulated in part by NLRP3 Inflammasome. Attenuation of inflammation is a major priority to prevent renal damage. Our previous publications show that DJ-1 has antioxidant and anti-inflammatory properties in the kidney. ND-13 is a short peptide consisting of 13 amino acids of the DJ-1-protein, which could increase DJ-1 pathway activation. The aim of these studies was to determine the role of NLRP3 in the pathogenesis of diabetic nephropathy and to study the possible renal protective effects of the DJ-1 pathway in diabetic mice and on inflammasome regulation. Bone marrow derived macrophages were treated with ND-13 and cultivated in high and low glucose. Diabetes was induced in C57Bl/6 mice via injection of streptozotocin and treated with ND-13 and MCC950, an inhibitor of the NLRP3 inflammasome. Peripheral mononuclear cells were isolated from human with diabetes, diabetic nephropathy and healthy donors and were plated, pretreated with ND-13 and stimulated with LPS+ATP. IL-1{beta} concentration in the medium of bone marrow derived macrophages increased by NLRP3 inflammasome stimulation by LPS+ATP, and decreased in macrophages pre-treated with ND-13, however, in the presence of LPS+Nigericin no effect was found. Peritoneal macrophages from diabetic mice were obtained and plated. Streptozotocin-induced diabetic C57BL/6 mice have increased the peritoneal cells IL-1{beta} production compared with control mice, suggesting that inflammasome may be activated in macrophages during diabetes and that ND-13 treatment normalized its activity. ND-13 and MCC950 decreased histologic evidence of tubular injury in STZ-induced diabetes in mice, additionally, significantly increased the mRNA expression of Col-I, Col-II, Tgf-{beta}, Il-6, Tnf- and P2x7 in the renal cortex, which was partially prevented by ND-13 and MCC950 pre-treatment. P2x7 mRNA expression was also increased in peritoneal macrophages obtained from diabetic mice, and its expression was attenuated by ND-13 pre-treatment. Peripheral mononuclear cells isolated from patients blood were plated and stimulated with LPS+ATP. Patients with diabetic nephropathy presented a significant increase of IL-1{beta} release compared to diabetic individuals and ND-13 could has a role in the prevention of inflammasome activation in healthy patients. Our results demonstrate that activation of the DJ-1 pathway is a promising approach to prevent renal inflammation and fibrosis during diabetes, by ameliorating inflammasome activation in peripheral immune cells. Thus, ND-13 could be a promising new therapeutic approach to attenuating inflammation and renal damage in diabetic nephropathy.

cell biology↗