(), a parasitic intracellular protozoan, can establish a chronic infection in the host brain and cause significant neuropathology. The current study aimed to determine the role of Tyrosine Hydroxylase (TH), Dopamine Receptor D1 (D1R), Nuclear Receptor Related-1 (Nurr1), and Dopamine Transporter (DAT) expression in the neuroimmunopathogenesis of toxoplasmic encephalitis (TE) at 15, 30, 45, and 60 days after infection with . Additionally, the study investigated whether there was a correlation between the markers on these critical days, which had yet to be explored. The results showed that TH expression in brain tissue of BALB/c mice was significantly increased in all infected groups compared with healthy controls (<0.05). However, other striking findings of the study were that D1R, DAT, and Nurr1 expression were significantly decreased in all infected groups compared with healthy controls, in contrast to TH expression (<0.05). Study findings regarding behavioral changes in chronic -infected laboratory animals and humans with TE provide important evidence of the relationship between neuropsychiatric diseases and infection. By elucidating the pathogenesis of the disease in detail, treatment protocols that consider these coordinated changes in expression that vary from day to day can be developed.
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http://dx.doi.org/10.14670/HH-18-877 | DOI Listing |
Histol Histopathol
January 2025
Department of Medical Pathology, Faculty of Medicine, Ankara Medipol University, Ankara, Turkey.
(), a parasitic intracellular protozoan, can establish a chronic infection in the host brain and cause significant neuropathology. The current study aimed to determine the role of Tyrosine Hydroxylase (TH), Dopamine Receptor D1 (D1R), Nuclear Receptor Related-1 (Nurr1), and Dopamine Transporter (DAT) expression in the neuroimmunopathogenesis of toxoplasmic encephalitis (TE) at 15, 30, 45, and 60 days after infection with . Additionally, the study investigated whether there was a correlation between the markers on these critical days, which had yet to be explored.
View Article and Find Full Text PDFVet Parasitol Reg Stud Reports
January 2025
Department of Microbiology & Immunology, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853, USA; Department of Public and Ecosystem Health, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853, USA; Feline Health Center, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853, USA. Electronic address:
Toxoplasmal meningoencephalitis is a sporadic condition that is often misdiagnosed antemortem, frequently resulting in euthanasia especially in resource-limited settings. Here we report a case of a 7-week-old female domestic shorthair cat from an animal shelter who presented in a compromised condition and continued to display clinical signs consistent with a "failure to thrive" kitten. Weight loss and decreased activity were observed, and later on, neurological dysfunction became apparent.
View Article and Find Full Text PDFZhong Nan Da Xue Xue Bao Yi Xue Ban
August 2024
Department of Parasitology, School of Basic Medical Sciences, Central South University, Changsha 410013.
Objectives: Toxoplasmosis is a zoonotic parasitic disease caused by (), which can lead to complications such as encephalitis and ocular toxoplasmosis. The disease becomes more severe when the host's immune system is compromised. Rhoptry proteins are major virulence factors that enable to invade host cells.
View Article and Find Full Text PDFBrain Sci
December 2024
College of Life Science and Engineering, Foshan University, 18 Jiangwan Street, Foshan 528231, China.
(), an obligate food-borne intracellular parasite, causes severe neuropathology by establishing a persistent infection in the host brain. We have previously shown that infection induces severe neuropathology in the brain manifested by increased nitric oxide production, oxidative stress, glial activation/BBB damage, increased pro-inflammatory cytokine glia maturation factor-beta and induced apoptosis. The aim of this experimental study was to investigate the serum amyloid P (SAP) components, nuclear factor kappa B (NF-κB), interleukin-1 beta (IL-1β), caspase 1 (Casp 1), tumor necrosis factor-alpha (TNF-α) and complement 3 (C3) gene expressions on the 10th, 20th and 30th days after infection with in the neuroimmunopathogenesis of toxoplasmic encephalitis (TE) in mouse brains by real-time quantitative polymerase chain reaction.
View Article and Find Full Text PDFSci Rep
January 2025
Department of Zoonotic Diseases, National Research Centre, Dokki, Giza, 12622, Egypt.
Toxoplasmosis induced by Toxoplasma gondii is a well-known health threat, that prompts fatal encephalitis increased with immunocompromised patients, in addition, it can cause chorioretinitis, microcephaly, stillbirth in the fetus and even led to death. Standard therapy uses sulfadiazine and pyrimethamine drugs revealed beneficial results during the acute stage, however, it has severe side effects. UPLC-ESI-MS/MS used to explore C.
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