The ability of immune rats to resist challenge with Babesia divergens depends upon mechanisms which are largely spleen independent. The possible removal of B. divergens PREC's by the livers of immune splenectomised rats was investigated. The clearance of Cr51 labeled B. divergens infected erythrocytes was followed in splenectomised rats to test whether Cr51 labeled PREC's are cleared from the circulation of immune rats through uptake and phagocytosis by the liver. No significant difference was observed between the clearance radioactivity from the circulation as well as the liver uptake in the immune rats from the controls. The uptake of infected erythrocytes by the liver is unlikely to happen in immune rats. Other unknown mechanisms appear to take part in clearing the parasitaemia in these rats. This might depend upon antibody inhibition of merozoite invasion. The injection of irradiated parasites into the same rats showed that they were able to clear PRBC's from the blood stream and that immunity was not specifically directed at merozoites. It is speculated that parasites inside red cells are removed by lysis or phagocytosis. Histological studies on livers collected from immune rats showed that lymphocytes are accumulated in the Liver and these consisted of B & T cells leukocytes accumulating in the liver might therefore be very important in the development of acquired immunity to B. divergens in splenectomised rats.
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Toxicol Pathol
December 2024
AbbVie Inc., North Chicago, Illinois, USA.
Enhanced histopathology of the immune system uses a precise, compartment-specific, and semi-quantitative evaluation of lymphoid organs in toxicology studies. The assessment of lymphocyte populations in tissues is subject to sampling variability and limited distinctive cytologic features of lymphocyte subpopulations as seen with hematoxylin and eosin (H&E) staining. Although immunohistochemistry is necessary for definitive characterization of T- and B-cell compartments, routine toxicologic assessments are based solely on H&E slides.
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December 2024
Instituto de Investigaciones Cerebrales, Universidad Veracruzana, Avenida Luis Castelazo s/n Col. Industrial Ánimas, Xalapa, Veracruz C. P. 91190. Mexico.
The pubertal phase involves significant brain reorganization, where external stressors and diet can profoundly influence long-term behavioral outcomes. In this study, we investigated the interaction between acute pubertal stress (via immune challenge) and a hypercaloric diet in adulthood on the copulatory sexual behavior of male Wistar rats. At postnatal day (PND) 35, pubertal males received a single injection of lipopolysaccharide (LPS, 1.
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December 2024
School of Pharmacy, Bengbu Medical University, No. 2600 Donghai Avenue, Bengbu 233000, Anhui, China; Anhui Engineering Technology Research Center of Biochemical Pharmaceutical, Bengbu, China. Electronic address:
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Cancer Research Unit, Sumitomo Pharma Co Ltd, Osaka, Japan. Electronic address:
Toll-like receptors (TLRs) are crucial for the detection of infections and activation of downstream signaling pathways that lead to the production of pro-inflammatory cytokines and interferons. Because of their strong immunostimulatory activity, TLRs are thought to be a "double-edged sword" for systemic treatment, even in the cancer field. To solve this, we have developed dextran-based TAM targeting activator conjugate (D-TAC) technology which successfully uses tumor-associated macrophages (TAMs) to deliver the TLR7 agonist DSP-0509.
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Zoology Department, Faculty of Science, Al-Azhar University, Cairo 11884, Egypt.
Background/aims: Gestational Diabetes Mellitus (GDM), a prevalent complication in pregnancy, is characterized by the Diabetes Association as diabetes diagnosed in the second or third trimester, often remaining asymptomatic. This study investigates the intricate effects of Streptozotocin on pregnant rats, unraveling its impact on Gestational Type 2 Diabetes (GTD). The research delves into the potential therapeutic roles of mesenchymal stem cells (MSCs) and olive leaf extract (OLE) in mitigating the consequences of Streptozotocin-induced pancreatic impairment.
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