Astrocytes, microglia/macrophages, and neurons expressing Toll-like receptor 11 contribute to innate immunity against encephalitic Toxoplasma gondii infection

Experimental Parasitology

2015

Section: Discussionmentioning

confidence: 99%

“…The low-virulence ME-49 strain of T. gondii was used for infection as previously described by Atmaca et al (Atmaca et al, 2014). Tissue cysts of T. gondii were harvested from the brains of mice that had been intraperitoneally inoculated with 20 cysts.…”

Section: Animal Infection Modelmentioning

confidence: 99%

Nitric oxide production increases during Toxoplasma gondii encephalitis in mice

Experimental Parasitology

2015

“…The low‐virulence ME‐49 strain of T . gondii was used for infection as previously described by Atmaca et al . Tissue cysts of T .…”

Section: Methodsmentioning

confidence: 99%

Increased expressions of ADAMTS‐13 and apoptosis contribute to neuropathology during Toxoplasma gondii encephalitis in mice

2015

Neuropathology

Toxoplasma gondii (T. gondii) is a protozoan parasite with the potential of causing severe encephalitis among immunocompromised humans and animals. Our previous study showed that T. gondii induces high nitric oxide (NO) production, high glial activation (GFAP) and neurofilament expressions, leading to severe neurodegeneration in toxoplasma encephalitis (TE) in the central nervous system (CNS). The aim of this experimental study was to investigate ADAMTS-13 expression and apoptosis in CNS and to identify whether they have any correlation with toxoplasmosis neuropathology and neurodegeneration. Mice were infected with ME49 strain T. gondii and the levels of ADAMTS-13, caspase 3, caspase 8, caspase 9, TNFR1 and Bcl-xL expressions were examined in brain tissues by immunohistochemistry, during the development and establishment of chronic infections at 10, 30 and 60 days post-infection. Results of the study revealed that the levels of ADAMTS-13 (P < 0.005), caspase 3 (P < 0.05), caspase 8 (P < 0.05), caspase 9 (P < 0.005) and TNFR1 (P < 0.05) expressions in the brain markedly increased while Bcl-xL expression decreased (P < 0.005). The most prominent finding from our study was that 10, 30 and 60 days post-infection ADAMTS-13 increased significantly and this may play an important role in the regulation and protection of the blood-brain barrier integrity and CNS microenvironment in TE. These results also suggest that T. gondii-mediated apoptosis might play a pivotal role and a different type of role in the mechanism of neurodegeneration and neuropathology in the process of TE. Furthermore, expression of ADAMTS-13 might give an idea of the progress and is critical for diagnosis of this disease. To the best of the authors' knowledge, this is the first report on ADAMTS-13 expression in the CNS of T. gondii-infected mice.

show abstract

“…The lowvirulence ME-49 strain of T. gondii was used for infection as previously described by Atmaca et al 12 Tissue cysts of T. gondii were harvested from the brains of mice that had been intraperitoneally inoculated with 20 tissue cysts. For experimental infection, mice were intraperitoneally inoculated with 15-20 ME-49 tissue cysts suspended in 0.25 mL of sterile physiologic saline.…”

Section: Animal Infection Model and Experimental Proceduresmentioning

confidence: 99%

Role of oxidative stress in the pathophysiology of Toxoplasma gondii infection

Int J Immunopathol Pharmacol

2016